MEDICAL SERVICES - WhatDoTheyKnow

Training & Development

Neurological Update

MED-CMEP~119

Version: 3 Final

23 April 2013

MEDICAL SERVICES

PROVIDED ON BEHALF OF THE DEPARTMENT FOR WORK AND PENSIONS

Self-Directed Learning Pack (for all Registered Medical Practitioners and

Registered Physiotherapists)

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Neurological Update 3 Final

MED -CME~119 Page 2

Foreword

This training has been produced as part of a training programme for Health Care Professionals (HCPs) approved by the Department for Work and Pensions Chief Medical Adviser to carry out benefit assessment work.

All HCPs undertaking assessments must be registered practitioners who in addition, have undergone training in disability assessment medicine and specific training in the relevant benefit areas. The training includes theory training in a classroom setting, supervised practical training, and a demonstration of understanding as assessed by quality audit.

This training must be read with the understanding that, as experienced practitioners, the HCPs will have detailed knowledge of the principles and practice of relevant diagnostic techniques; therefore such information is not contained in this training module.

In addition, the training module is not a stand-alone document, and forms only a part of the training and written documentation that the HCP receives. As disability assessment is a practical occupation, much of the guidance also involves verbal information and coaching.

Thus, although the training module may be of interest to non-medical readers, it must be remembered that some of the information may not be readily understood without background medical knowledge and an awareness of the other training given to HCPs.

Office of the Chief Medical Adviser

April 2013

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Document control

Superseded documents

Version history

Version Date Comments

1 Final 25 January 2011 Signed off by CMMS

2a draft 23 January 2012 Schedule 28 Review and amendments Medical Training & Development

2 Final 22 February 2012 Signed off by CMMS

3a Draft 27 March 2013 Schedule 28 update by xxxxxxxx

3 Final 23 April 2013 Signed off by HWD and CMMS

Changes since last version

Foreword updated

References to ‘Medical Manager’ changed to ‘Clinical Manager’

Typos corrected

Page 61: NMC added to list of professional bodies

Observation form: Title of xxxxxxxxxupdated

Outstanding issues and omissions

Updates to Standards incorporated

Issue control

Author: Dr A H based on previous Atos Healthcare material

Owner and approver: National Clinical Manager (Performance)

Signature: Date:

Distribution:

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Contents

Introduction 7

An introduction to your Learning Pack 7

A guide to using this pack 7

Background to this Learning Pack 8

Section One – Neuroanatomy and Neurophysiology 9

Objectives 9

Duration 9

Cells, Neurons and Neuromuscular Junctions 9

Central Nervous System 10

Peripheral Nervous System 13

Autonomic Nervous System 17

From recall, or review of diagrams on Page 15, you should have responded as follows: 18

Reflexes 18

Upper Motor Neuron versus Lower Motor Neuron Lesions 19

Section Two - Neurological Examination 21

Objectives 21

Duration 21

History 21

Observation 22

Examination 23

Inspection 23

Testing the Motor System 23

Tone 23

Power 24

Reflexes 25

Testing the Sensory system 29

Section Three - Specific Conditions 34

Objectives 34

Duration 34

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Prolapsed Intervertebral Disc and Sciatica 35

Cause 35

Symptoms and Signs 36

Treatment 37

Functional impact 37

Cervical Spondylosis 39

Cause 39


Treatment 40


Peripheral Neuropathy 42

Cause 42

Diabetes 42

Alcohol misuse 43


Treatment 45


Nerve Compression Syndromes and Focal Neuropathy 47

Median nerve (carpal tunnel syndrome) 47


Treatment 49


Ulnar Nerve 49


Treatment 50


Radial Nerve 50


Treatment 52


Common Peroneal Nerve 52


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Treatment 52

Functional Impact 53

Lateral Cutaneous Nerve of the Thigh 53


Treatment 53


Brachial Plexus Injuries 54

Symptoms and signs 54

Treatment 54


Thoracic Outlet Syndrome 55


Treatment 55


Raynaud’s Phenomenon, Hand-Arm Vibration Syndrome and Vibration White Finger 59

Raynaud’s Phenomenon Error! Bookmark not defined.

Hand-Arm Vibration Syndrome (HAVS) 60

Vibration White Finger (VWF) 60


Further Reading 61

Section Four – Multiple Choice Questionnaire 62

Duration 62

Neurological Update MCQ 63

Glossary 66

Observation Form 72

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Introduction

An introduction to your Learning Pack

Welcome to this ‘Neurological Update’ distance learning module for registered medical practitioners (either employed, or self-employed) and registered physiotherapists. The Learning Pack will take you approximately 3 hours to complete, which can be done in one go or at smaller separate “sittings”. It is important that you complete learning activities in the order they are given; by doing so you will reflect, consolidate and build on your learning throughout. You will be asked to interact at various stages during this learning opportunity – writing your responses in the boxes provided – all answers will be found in the body of text, but you should first attempt to recall information before finally reviewing the main body of text to check for definitive answers.

Your knowledge and understanding will be further tested by an MCQ, at the end. The completed MCQ must be returned to the Clinical Manager at your local Medical Services Centre (MSC) for marking. The pass mark is 85% or above. If you achieve less than 85%, the Clinical Manager will ask you to read the documents again and then repeat the MCQ,

A guide to using this pack

The following symbols are used to assist you in completing the learning activities included in this folder.

Indicates a time for reading

Indicates you should record / write your views and comments

Duration

Suggests the approximate time needed to complete any particular learning activity

Learning Pack Objectives

Through completion of this learning pack you should enhance your existing knowledge of:

Neuroanatomy and neurophysiology

Neurological examinations required in the context of disability assessments

Specific neurological conditions

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Background to this Learning Pack

Neurological symptoms and conditions are common; approximately 10% of GP consultations are about a neurological symptom. In our role as Disability Analysts, roughly 20% of ESA cases examined have a neurological symptom or problem.

The nervous system is the most elaborate bodily system. The field of neurology is correspondingly vast and complex. Neurological conditions can range from the simple to the highly complicated. The neurological system is therefore one of the most difficult systems to fully examine.

The focus for this training will be on some of the more common neurological conditions that are seen within our sphere of work.

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Section One – Neuroanatomy and Neurophysiology

Welcome to the first section of your Learning Pack, which contains an overview of the principles of basic neuroanatomy and neurophysiology. The site of a lesion or problem within the neuromuscular system will often lead to a characteristic set of signs and symptoms. Therefore refreshing your knowledge of these principles will assist you assessing neurological cases in your role as a Disability Analyst.

Objectives

By the end of this section, you will have refreshed your knowledge of:

Basic neuroanatomy concepts

Basic neurophysiology concepts

Dermatomes and myotomes

The difference between the terms ‘upper’ and ‘lower’ motor neuron(s)

Duration

The learning activities during this section should take approximately 50 minutes to complete.

Cells, Neurons and Neuromuscular Junctions

The neuron is the anatomic and functional building block of the nervous system - each one is composed of a cell body; dendrites (processes leading towards the cell body); and axons (processes leading away from the cell body). Other cells in the nervous system (astrocytes, oligodendrocytes and microglial cells) play a ‘support’ role.

A neuron

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Many neurons have myelin sheaths (‘myelinated’ neurons) composed of specialised cells called Schwann cells. These wrap around the axon acting as insulation, and so assist in the conduction of electrical impulses.

A myelinated neuron

Synapses (contacts between cells allowing transmission of signals) use chemical ‘neurotransmitters’ for communication (e.g. dopamine and serotonin). Some synapses are excitatory (making a nerve cell more likely to produce and carry an impulse); some are inhibitory (making a nerve cell less likely to produce and carry an impulse).

Communication from a neuron to a voluntary (skeletal muscle) cell occurs at the motor end plate (also known as myoneural junction). One motor neuron usually supplies a number of muscles cells (known as a motor unit).

Central Nervous System

The central nervous system (CNS) consists of the brain and the spinal cord. The brain is made up of the cerebrum, cerebellum and brain stem.

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Lateral view of the brain

The cerebrum consists of the right and left cerebral hemispheres. It is concerned with cognition, the higher (voluntary) control of movement, perception of sensation (touch, pain, pressure and temperature), vision and hearing. The concept of cerebral dominance arose with a simple observation: right-handed stroke patients with acquired language disorders had destructive lesions within the left hemisphere. Almost all right-handed, and 70% of left-handed, people have language function in the left hemisphere. Destructive lesions within the left fronto-temporo-parietal region cause various disorders of human communication: in spoken language (aphasia/ dysphasia), in writing (agraphia), and/ or in reading (acquired alexia). Aphasia (lost/ defective language from damage to speech centres within left hemisphere) can be of numerous types, not least Broca’s or ‘expressive’ aphasia – where there is reduced fluency of speech but preservation of comprehension. There is failure to construct sentences, and people who recover from this form of aphasia say they knew what they wanted to say, but “could not get the words out”. In Wernicke’s or ‘receptive’ aphasia language is fluent but the words themselves are incorrect – this varies from insertion of a few incorrect words into fluent speech, to a profuse outpouring of jargon (which may be confused with psychotic behaviour). People who have recovered from this say that when aphasic they found speech, both their own and others, “like a wholly unintelligible foreign language”.

The following table summarises some of the disorders that can arise from lesions in the various regions of the cerebral cortex:

FRONTAL CORTEX OCCIPITAL CORTEX

TEMPORAL CORTEX PARIETAL CORTEX

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Table: Principle features of destructive cortical lesions (in a right-handed individual)

Site of lesion Disorder

Frontal (either side) Intellectual impairment; personality change; urinary incontinence; monoparesis or hemiparesis

Frontal (left side) Broca’s aphasia

Temporo-parietal (left side) Acalculia; alexia; agraphia; Wernicke’s aphasia; right-left disorientation; homonymous field defect (where visual field to one side of body is restricted in both eyes)

Temporal (right side) Confusional states; failure to recognise faces; homonymous field defect

Parietal (either side) Contralateral sensory loss or neglect; agraphaesthesia (difficulty recognising a number/ letter traced on palm of hand)

Parietal (right side) Dressing apraxia (inability to execute learned purposeful movements, despite having the desire and physical ability to perform them); failure to recognise faces

Parietal (left side) Limb apraxia

Occipital/ occipitoparietal Visual field defects; visuospatial defects; disturbances of visual recognition

The cerebellum operates at an unconscious level. It controls muscle tone and posture and the co-ordination of movement.

The brainstem contains centres controlling vital functions including respiration, the cardiovascular system and level of consciousness. It is also the origin of many of the cranial nerves.

The spinal cord occupies the vertebral canal enclosed within the vertebral bodies. It is continuous with the brainstem. It provides sensory, motor and autonomic innervation for the trunk and limbs. Within the spinal cord and brainstem, nerves sharing common functions often follow the same course, known as tracts. There are ascending sensory tracts going to the brain from the periphery and descending motor tracts going away from the brain to the periphery.

Broadly speaking, most of the sensory and motor tracts within the CNS cross to the other side. This is known as decussation. Therefore, the left cerebral hemisphere perceives sensations and controls movement of the right side of the body and the right cerebral hemisphere perceives sensations and controls movement of the left side of the body.

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Different nerve tracts decussate at different levels of the CNS. The main motor tracts decussate in the brainstem, therefore lesions in the brain and higher brain stem will cause problems on the opposite side of the body. Lesions of the motor tracts in the spinal cord will cause problems on the same side of the body.

Lesions of the spinal cord may produce two effects, firstly by causing loss of function at a local (segmental) level; and secondly by damaging descending motor or ascending sensory tracts. The principle ascending sensory tracts include the posterior columns – whose axons carry the sensory modalities of vibration sense, joint position (proprioception), light touch and two-point discrimination; and the spinothalamic tracts – whose axons carry pain and temperature sensation. Whereas the posterior columns remain uncrossed until the medulla (lowest part of the brainstem), the spinothalamic tracts cross over the midline close to their entry into the spinal cord.

Posterior column lesions can present with tingling, electric-shock-like sensations, clumsiness, and numbness. These symptoms, though lateralised, are often felt vaguely and without a clear sensory level. On examination, position sense, vibration sense, light touch and two-point discrimination are lost below the lesion. Loss of position sense produces the stamping gait of sensory ataxia.

Spinothalamic tract lesions cause contralateral loss of pain and temperature sensation with a clear level below the lesion. This is called ‘dissociated sensory loss’ – pain and temperature are dissociated from light touch, which remains preserved. This is seen typically in the condition syringomyelia where a cavity occupies the central spinal cord. Because spinothalamic tract lesions cause loss of pain and temperature perception, they can result in potentially serious problems such as painless burns. Perforating ulcers and neuropathic joints (Charcot joints) can also develop.

Peripheral Nervous System

The peripheral nervous system is made up of the cranial and spinal nerves. There are twelve paired cranial nerves. HCPs who are registered nurses or physiotherapists do not assess conditions involving problems with the cranial nerves. If you are a registered medical practitioner, such cases may be ‘handed over’ to you from your nursing and physiotherapist colleagues – and although these cases are few and far between, it is important to refresh your knowledge on the core functions of each of the cranial nerves.

The table below summarises these:

Cranial nerve No.

Name Main action

I Olfactory Smell

II Optic Vision, fields, afferent light reflex

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III Oculomotor Eyelid elevation, eye elevation, Adduction, depression in Abduction, efferent (pupil)

IV Trochclear Eye intorsion, depression in Adduction

V Trigeminal Facial and corneal sensation, muscles of mastication

VI Abducens Eye Abduction

VII Facial Facial movement, taste fibres

VIII Vestibular

Cochlear

Balance

Hearing

IX Glossopharyngeal

Sensation – soft palate, taste fibres

X Vagus Cough, palatal and vocal cord movements

XI Accessory Head turning, shoulder shrugging

XII Hypoglossal Tongue movement

There are 31 paired spinal nerves (8 cervical, 12 thoracic, 5 lumbar, 5 sacral and 1 coccygeal). Each segment of the spine gives off a ventral and dorsal root bilaterally. These unite in the intervertebral foramen to form a spinal nerve.

Ariel view of spinal vertebral neuroanatomy

The spinal cord ends at the level of the first lumbar vertebrae (L1). At this level the cord separates into the separate lumbar and sacral spinal nerves, known as the cauda equina (‘horses tail’), that continue down the vertebral canal to their exit points.

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Each spinal nerve contains sensory innervation for part of the body surface. This area of skin is known as a dermatome.

Dermatome chart

Note, these areas are only approximate; as adjacent spinal nerves do overlap (you may find minor variations between dermatome charts from different sources). All areas of the skin receive fibres from more than one spinal nerve, therefore damage to a single spinal nerve may cause little or no sensory loss.

In the region of the upper limbs and lower limbs the spinal nerves become redistributed within a nerve plexus to create peripheral nerves. Therefore the distribution of peripheral nerves is different from spinal nerves. The upper limb plexus is the brachial plexus, which is located bilaterally in the axilla and neck. The lower limb plexus is the lumbosacral plexus, which is located bilaterally within the pelvis.

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Peripheral nerves can become compressed and this leads to specific symptoms and signs based on the nerve involved.

The group of skeletal muscles innervated by a spinal nerve is known as a myotome. These muscles are responsible for specific patterns of movement. The following illustrations demonstrate the segmental innervation of the main limb movements:

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The sensory system is concerned with the sensations of pain, touch, temperature and proprioception. There are different receptors within the skin for pain, temperature, light touch, discriminative touch and vibration.

Referred pain is pain felt at a site distant from the tissues causing the pain. It can be referred to the surface or deep within the body. It is often associated with pain from internal organs and may be felt at a site of the body which is far removed from its source (e.g. diaphragmatic pain can be felt in the tip of the shoulder, and cardiac pain in the left shoulder). Referred pain from the ligaments and muscles of the spinal column can also be felt at remote sites in the upper and lower limbs.

Autonomic Nervous System

The autonomic nervous system (ANS) contains neurons within both the CNS and peripheral nervous system that control the internal (visceral) organs, smooth and cardiac muscle, and the glands of the body. It is primarily concerned with the control of internal environment and functions at a subconscious level.

The neurons of the autonomic nervous system are divided into two functional groups: sympathetic nerves, and parasympathetic nerves. Most structures that are innervated by the autonomic nervous system are innervated by both types of nerves which exert opposite effects on that structure.

Stimulation of the sympathetic system produces the ‘fight and flight’ response, which includes the following effects: tachycardia, decreased salivation, decreased bowel motility, increased sweating, inhibition of micturition, and dilatation of bronchi.

Stimulation of the parasympathetic system generally produces the opposite effects, including: bradycardia, increased bowel motility, initiation of micturition, and constriction of the bronchi.

Interaction: Try to recall the segmental innervation(s) which control(s) the following movements:

Knee flexion Knee extension

Hip flexion Hip extension

Ankle plantarflexion Ankle dorsiflexion

Wrist flexion Wrist extension

Elbow flexion Elbow extension

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From recall, or review of diagrams on Page 15, you should have responded as follows:

Knee flexion - L5, S1 Knee extension - L3, L4

Hip flexion - L1, L2, L3 Hip extension - L5, S1

Ankle dorsiflexion - L4, L5 Ankle plantarflexion - S1, S2

Wrist flexion - C6, C7 Wrist extension - C8

Elbow flexion - C5, C6 Elbow extension - C6, C7

Reflexes

A reflex is an involuntary pattern of response following a stimulus. Deep tendon reflexes are stretch reflexes - when a muscle is stretched it responds by contracting. It is the simplest of reflexes and mediated by a monosynaptic reflex arc. This simply means that the pathways of the reflex consist of only afferent sensory neurons carrying impulses from the muscle stretch and efferent motor neurons carrying impulses back to the stretched muscle, as well as an inhibitory effect to the antagonistic muscle.

Monosynaptic reflex arc

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Each of the commonly tested reflexes is sub-served by specific spinal cord segments:

Supinator (brachioradialis reflex) C5/C6

Triceps C6/C7 or C7/8

Biceps C5/C6

Knee (quadriceps) L3/L4

Ankle (Achilles tendon) S1/S2

A plantar reflex (also known as Babinski reflex) is a superficial rather than a deep tendon reflex. This has a much more complex pathway, but in summary, it provides information about the motor pathways to the lower limb. You will read more about reflexes in the neurological examination section.

Upper Motor Neuron versus Lower Motor Neuron Lesions

Neurological conditions will often be described as an upper motor neuron condition or a lower motor neuron condition. Lower motor neurons are those that directly innervate skeletal muscle. They are the final common pathway by which the nervous system controls movement. Upper motor neurons are located in descending tracts, which control the activity of the lower motor neurons. Upper motor neuron lesions can occur in the brain or spinal cord. Lower motor neuron lesions can occur in the nerve roots or peripheral nerves.

An upper motor neuron syndrome is usually characterised by the following:

Weakness or paralysis of specific movements (e.g. extension of upper limbs) also known as pyramidal weakness

Lack of any focal muscle wasting (unless there is prolonged disuse)

Increased resistance to passive stretching of muscles (spasticity)

Extensor (upwards) plantar reflex - if present, this is a definite sign of an upper motor neuron condition

Hyperactivity of deep tendon reflexes (hyperreflexia)

A lower motor neuron syndrome is usually characterised by the following:

Muscle wasting

Weakness (paresis) or paralysis (plegia) of individual muscles

Fasciculations (a brief flickering contraction seen in the belly of the muscle)

Reduced resistance to passive stretching (hypotonia)

Decreased or lost deep tendon reflexes (hyporeflexia)

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Interaction: Note down your answers to the following questions

What makes up the central nervous system?

What makes up the peripheral nervous system?

What makes up the autonomic nervous system?

What signs would you expect to see in an upper motor neuron lesion?

What signs would you expect to see in a lower motor neuron lesion?

Now re-review the information detailed in Section One, to check whether you have responded correctly.

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Section Two - Neurological Examination

The focus of this section will be on examination of the neurological system. However, it will also cover history and observed behaviour. In your role as a disability analyst assessing neurological cases, the importance of careful and focused history taking, recording of observed behaviour and specific neurological examination cannot be overstated. It is always important to consider all pieces of evidence obtained in the light of what is medically reasonable. Your opinion must be fully justified and supported by evidence and any inconsistencies between pieces of evidence must always be addressed.

Objectives

By the end of this section, you will have refreshed your knowledge of:

History taking in neurological cases

Observed behaviour in neurological cases

The principles of a focused neurological examination

Duration


History

The history of any given condition provides evidence, which is important in the formulation of your opinion. You should ask about the following:

Onset of the condition or problem

What symptoms the claimant experiences

Investigation and treatment thus far

Progress with treatment

With neurological conditions, it is very important to ask about the location of the symptoms experienced by the claimant. Depending on the medical condition reported, it may be appropriate to ask whether the claimant has other symptoms which they have not mentioned: such as paraesthesiae, numbness, weakness and/ or problems with micturition or continence.

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Observation

Observed behaviour remains a cornerstone of disability analysis. As always it is important to observe and record relevant informal observed behaviour such as sitting, standing, rising, use of arms, walking and getting on to and off the couch.

Neurological conditions can of course affect any or all of these activities. Gait and balance are commonly affected.

When assessing gait, the following should be considered:

Is the gait symmetrical or asymmetrical?

Is the size of steps normal, small or large?

Posture, is it upright (normal) or stooped?

Do the arms swing normally or is this reduced or increased?

What is the lateral distance between the feet is it normal or increased?

What is the position of the knees, are they being raised higher than normal?

What about the movement of the pelvis and shoulders, are they normal or reduced / exaggerated?

A normal gait is symmetrical, with normal sized steps and an upright posture. The distance between the feet is normal and the knees are raised to a normal height. Examples of abnormal gaits include:

Hemiplegic - asymmetrical gait, with one leg swinging to the side. Seen in upper motor neuron lesions, such as stroke and multiple sclerosis

Parkinsonian - symmetrical small stepped shuffling gait, stooped, difficulty starting and stopping. There are many causes including Parkinson’s disease, and as an effect of antipsychotic medication

Scissoring - symmetrical, feet cross over each other with toes dragging. Is an indication of spastic paresis and is seen in cord compression, cerebral palsy

High stepping - may be symmetrical or asymmetrical. Knee is raised higher than normal. Seen in bilateral or unilateral foot drop

Waddling - symmetrical, with excessive rotation of pelvis and shoulders. Is as a result of weak proximal muscles, causes include proximal myopathies, bilateral congenital dislocation of the hip

Antalgic - asymmetrical, claimant in pain, heavily reliant on non painful side, favouring non painful side

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Orthopaedic - asymmetrical, associated with bony defects, such as a shortened limb.

Ataxic - symmetrical wide based gait with irregular stride length, seen in cerebellar conditions and can be seen in peripheral neuropathy where joint position sense has been lost

Functional - may be symmetrical or asymmetrical, does not fit any recognised pattern, may get worse when known to be observed, not consistent with examination findings.

Examination

Inspection

As part of a regional neurological examination you should look for muscle wasting, ulceration, fasciculation (flickering contractions in belly of the muscle, which does not produce movement at a joint), trophic changes including ulceration, swelling of joints, malformation and signs of injury or surgery.

Testing the Motor System

Tone

When testing tone it is important that the claimant is relaxed. This can be difficult to ensure, especially as telling the claimant to relax often makes them tense up. It can help to distract the claimant by talking generally about irrelevancies or asking them to count back from 100. Be aware when testing tone in limbs with painful joints - check with the claimant before moving the limb.

In the upper limb, tone can be tested by taking the claimant’s hand and initially pronating the hand then flexing the elbow, followed by flexing and extending the wrist.

In the lower limb, tone can be tested by gently rotating the limb from side to side, then flexing knee and ankle joints.

With normal tone, there will be slight resistance throughout the whole range of movements. When tone is decreased, there is a loss of that slight resistance. If there is significant loss of tone, the limb will be termed flaccid. When tone is increased, there is increased resistance - this can be of several types:

Lead pipe rigidity, where resistance is increased throughout the entire range of movement

Cogwheel rigidity, where resistance breaks intermittently throughout whole range

Clasp knife rigidity, where after initial resistance to movement there is sudden reduction in tone and the limb moves freely throughout the rest of the range of the particular movement

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Reduced tone is seen in lower motor neuron lesions, cerebellar lesions and myopathies.

Clasp knife rigidity is seen in upper motor neuron lesions where spasticity is present. Lead pipe rigidity and cogwheel rigidity is seen in extra pyramidal syndromes (see glossary). Extra pyramidal disorders are classified broadly into akinetic-rigid syndromes, in which poverty of movement predominates (Parkinson’s disease is the commonest serious example of this); and dyskinesias, in which there are various excessive involuntary movements (e.g. Huntington’s disease, Sydenham’s chorea, myoclonus, benign essential tremor, Tourette’s syndrome, and spasmodic torticollis to name but a few examples).

Power

When examining power, consider what myotomes / spinal nerves / peripheral nerves you are actually testing for during each movement.

Conventional grading of power uses the Medical Research Council (MRC) scale. When grading power, the maximal power attained should be used, even if this is only sustained for a brief time.

5 Normal power

4 Movement against resistance

3 Moves against gravity but not resistance

2 Moves with gravity eliminated

1 Flicker of movement can be seen in body of the muscle

0 No movement

It is very important that any muscle weakness elicited during the examination is evaluated with other pieces of evidence. Is the weakness in an area that is consistent with the history? Are there corresponding changes in reflexes or tone? Can you consistently elicit the weakness or is it erratic? Is there a difference between the observed behaviour and formal examination findings? It is usually not appropriate to test specifically for any of Waddell’s Sign’s. If you observe that a claimant has no difficulty sitting with legs outstretched, however, and yet shows restricted Straight Leg Raising on examination, it would be important to document this.

A claimant who is able to rise from a chair without difficulty, walk normally and is able to get on and off the couch without difficulty is unlikely to have significant weakness in the lower limb.

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Reflexes

When testing reflexes it is important that the claimant is relaxed. Examination of reflexes cannot be performed unless the claimant is relaxed. As with tone, you may need to try to distract the claimant with conversation etc.

Reflexes can be graded using the following scale:

Absent

Present but reduced

Normal

Increased (brisk)

Clonus

Deep tendon reflexes are increased (brisk) in upper motor neuron lesions and reduced or absent in nerve root or peripheral nerve lesions and myopathies. Clonus is repetitive reflex contractions, most often seen in legs. Sudden dorsiflexion of the ankle joint will result in repetitive contractions. One or two beats of clonus can be normal, any more than 2 beats of clonus is always abnormal, and indicates substantially increased tone.

If reflexes are absent, before they can be confirmed as absent, reinforcement manoeuvres may be carried out. These include:

Clenching teeth together (in upper limbs)

Hands clenched together across chest with claimant attempting to pull them apart (in lower limbs)

Isolated absent tendon reflexes may be a normal finding. When using a tendon hammer, you should ensure it is held correctly and swung rather than being used in a stabbing motion.

a) Biceps reflex

This reflex tests the C5 and C6 nerve roots.

You will need to expose the upper arm so that the biceps muscle is visible. With the claimant sitting ask them to place their hand in their lap, or if they are lying, ask them to place their hand palm down on their abdomen. Lay your index finger or thumb on the biceps tendon and hit your finger with the tendon hammer. Laying your finger on the biceps tendon ensures the stimulus is adequately transferred to the tendon.

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Eliciting the biceps reflex: you should see a visible, and feel a palpable, contraction of biceps muscle

b) Triceps reflex

This reflex tests the C6-C8 nerve roots.

You will need to expose the upper arm so that the triceps muscle is visible. Ask the claimant to bring their arm across their chest. Hold the wrist so that the elbow is held at 90 degrees. Hit the triceps tendon with the tendon hammer.

Eliciting the triceps reflex: you should see visible contraction in the triceps muscle

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c) Supinator reflex (also known as Brachioradialis)

This reflex tests the C6 nerve root.

You will need to expose the lower arm so that the brachioradialis muscle is visible. With the claimant sitting, ask them to place their hand in their lap, or if they are lying, place their hand palm down on their abdomen. Lay your finger on the brachoradialis tendon 3-5cm above the wrist joint and strike your finger with the tendon hammer.

Eliciting the supinator reflex: you should see a visible and feel a palpable contraction of brachioradialis muscle

d) Knee reflex

This reflex tests the L3 and L4 nerve roots.

With the claimant lying down, place your arm under their knee drawing it up so that the knee is flexed to 90 degrees, with your arm supporting the weight of the leg. It is important that the claimant is relaxed. Strike the knee below the patella on the infrapatellar tendon with the tendon hammer. This can also be performed with the claimant sitting on the side of the couch, with knees at 90 degrees and lower legs dangling.

You should see a visible contraction of the quadriceps muscle, causing a jerk of the lower leg.

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e) Ankle reflex

This reflex tests S1 and S2 nerve roots.

It may be performed in several ways:

With the claimant lying down, externally rotate foot bending the knee slightly, then dorsiflex the foot gently to 90 degrees and strike Achilles tendon with the tendon hammer

Or

With the claimant lying down with their legs out straight, place your hand on the ball of the foot with the ankles at 90 degrees, strike your hand with the tendon hammer

Or

Ask claimant to kneel on a chair so that his ankles are hanging over the edge, and strike the Achilles tendon directly with tendon hammer. However, you should be especially careful when testing claimants in this position (and preferentially, you should seek to perform this test with the claimant lying down – whence there is less risk of unsteadiness).

You should see a visible contraction of the calf muscle. This reflex may be absent in people over 65y, however it is often absent because the tendon is not hit correctly or claimant is holding their foot rigidly in dorsiflexion.

f) Plantar reflex

To test a plantar reflex ask the claimant to remove their footwear including socks. They must be lying down and relaxed. You must explain to the claimant that you are about to stroke the bottom part of their foot, as it can be an unpleasant sensation.

Using the end of the tendon hammer, gently draw it up the lateral border of the foot and across the ball of the foot.

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Eliciting the plantar reflex: you should see movement of big toe and adduction (spreading) of the other toes. Downwards movement (plantarflexion) of the big toe is normal and upwards movement (dorsiflexion) is abnormal

An ‘extensor’ plantar response must be distinguished from withdrawal (the claimant may actively pull their foot away as the sensation is unpleasant). If there is no movement of the big toe, check that the metatarsophalangeal joint has not been arthrodesed (fused).

Testing the Sensory system

The following sensory modalities are tested because they are easy to test and provide information that can help identify the site of neuropathology. In the CNS, vibration, joint position and touch afferent fibres travel in a tract in the posterior spinal cord. With spinal cord lesions, these sensory modalities may be lost individually, totally, or in certain combinations, depending on the site of the lesion; whereas sensory loss from interruption of a peripheral nerve or posterior spinal root affects all modalities.

When testing sensation it is important that you explain to the claimant what the test involves and what they are expected to do. They must understand the instructions to produce accurate consistent results. You may need to check their understanding before performing the test. Sensory signs are less objective than motor or reflex signs. The following sections describe testing of the different sensory modalities.

Vibration

Vibration sense is tested using a tuning fork. First explain to the claimant that they are being asked whether they feel vibration. Demonstrate initially by striking the tuning fork and placing it on their chin or sternum whilst vibrating and still. Do ensure they understand that it is the vibration they are feeling not just the contact on the skin of the tuning fork.

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Then ask the claimant to close their eyes. Strike the tuning fork and place it on the most distal joint of the limb, and ask the claimant if they feel any vibration. If is not felt then move to the next more proximal joint and so on until buzzing is felt.

In the lower limb start with the tip of the big toe, then the first metatarsophalangeal joint, then medial malleolus at the ankle, the tibial tuberosity just below the knee and the anterior superior iliac spine just above the hip.

In the upper limb begin with the tip of the index finger, then in ascending order each interphalangeal joint of the index finger, the second metacarpophalangeal joint, the ulnar styloid at the wrist, the medial epicondyle of the elbow and the tip of the acromium at the shoulder.

Joint position (proprioception)

Again, it is very important to explain to the claimant exactly how the test will be performed and what is expected of them. This is best done by initially demonstrating the test with the claimant being able to view the joint. Holding the sides of the distal part of the joint (so that they are not simply feeling the pressure of your touch), move it down and up, telling the claimant which direction the movement is in.

Once they understand, ask them to close their eyes. Start distally and if there is abnormal position sense move proximally. If the most distal joint tested is normal, then it will be normal proximally.

In the lower limb check the metatarsophalangeal joints. In the upper limb examine the interphalangeal joints and metacarpophalangeal joints.

Normally people are able to detect minimal movement at a joint. Where there is a loss of position sense they may be unable to feel any movement, or they may be unable to state the direction (i.e. they may think that movement has been up when in fact it has been down).

Romberg’s test is a test of joint position sense. It cannot be performed if a claimant is unable to stand unaided or is unable to remain standing steadily with their eyes open.

Ask claimant to stand with their feet together. After a few seconds, if there is no problem standing, ask them to close their eyes.

The claimant may fall during the performance of this test. Advise the claimant that you are ready to steady them and prevent their falling (and be ready to do so).

Note that it takes some moments to develop with increasing amplitude of slow swaying, until claimant can no longer remain upright. Claimants who immediately fall in one direction after closing their eyes do not have a positive Romberg’s test.

Light touch

This is usually performed lightly touching the skin using a piece of cotton wool or tissue, although it can be done using your fingertip. It is important to try to avoid a predictable stimulus. If using a fingertip do not drag your finger across the skin.

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Demonstrate what is required. Ask claimant to say yes each time they feel a touch. Once the claimant understands, perform the test with their eyes closed.

Start distally and move proximally. Check both sides. Do it randomly at different time intervals. If there is an abnormal result then starting at this point, check outwards to delineate the area of abnormal sensation.

Sacral sensation is not checked in disability assessment. It may be abnormal in people with bladder and bowel symptoms, bilateral leg weakness or sensory loss. However, this would be regarded as an intimate assessment and therefore should not be performed in this setting.

Pin prick

Examination of pinprick sensation is not performed within our disability assessments.

Temperature

Examination of temperature sensation is not performed within our disability assessments.

Two Point Discrimination

Examination of two-point discrimination sensation is not considered here, as it is unlikely to add any significant functional information to the tests outlined above.

Coordination

Coordination of movement requires integration of the sensory and motor systems. Problems with coordination are mainly seen with cerebellar disease (causing ‘cerebellar’ ataxia); but are also seen when there is abnormality of joint position sensation (loss of proprioception).

Dysdiadochokinesis is the inability to execute rapidly alternating movements (particularly of the limbs), and thought to be caused by the failure to ‘switch on’ and ‘switch off’ antagonising muscle groups It is a feature of cerebellar ataxia and, amongst other conditions, is seen in multiple sclerosis and Friedreich’s Ataxia. Slow or awkward movements (ipsilateral to the side of the cerebellar lesion) are classic. Lower limbs normally perform less well than upper limbs.

Upper limb coordination can be tested with the finger – nose test. Hold your finger out at arm’s length from claimant and ask the claimant to touch their finger tip to yours, then to their nose, then back to your finger etc, moving your finger to different positions. When it has been done correctly ask them to repeat it faster (the claimants arm has to be stretched out fully to examiner’s finger for the test to be sensitive). Look for accuracy and smoothness of movement. Be aware claimants may have difficulty performing this test if they have limb weakness or arthropathy. Difficulty performing this test indicates cerebellar disease or sensory ataxia which is loss of proprioceptive feedback.

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In the lower limb coordination can be tested with the heel - shin test. With the claimant laying down on the couch, ask them to lift their leg and place the heel on the knee of the opposite leg, then run it down the sharp border of the calf. It may be necessary to demonstrate what is required. Again watch for accuracy and smoothness of movement. Be aware claimants may have difficulty performing this test if they have limb weakness or arthropathy.

Abnormal movements

Claimants with neurological conditions where involuntary abnormal movements feature, should be assessed by HCPs who are registered medical practitioners. Abnormal movements that may be seen in the disability assessment setting include:

a) Tremor - repetitive rhythmical movement of the body or part of the body

b) Chorea - constant rapid complex body movements that appear pseudo-purposeful but are involuntary

c) Tardive dyskinesia - characterised by repetitive, purposeless movements, which are involuntary and include grimacing, tongue protrusion, lip smacking, puckering and pursing, and rapid eye blinking. Rapid movements of the arms, legs, and trunk may also be seen. This is often seen as a side effect of long-term use of the older anti-psychotic medications

d) Dystonia - prolonged muscle contraction, resulting in twisting body motions, abnormal posture. May involve the whole body or specific parts

e) Myoclonic jerk - very brief contraction of a muscle group, causing involuntary jerk of limb. It occurs normally sometimes as people are dropping off to sleep.

In summary, this section has covered the basics of history, observed behaviour and examination of claimants with neurological conditions or symptoms. The importance of applying logical reasoning to all of the pieces of evidence obtained during the assessment cannot be overstated. As always, your justification should address any inconsistencies between the various pieces of evidence.

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Interaction: What spinal segments do the following reflexes subserve?

Biceps

Triceps

Supinator

Knee

Ankle

Plantar

Now re-review the information detailed in Section Two to check whether you have responded correctly.

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Section Three - Specific Conditions

This section provides information about the neurological conditions that you are most likely to see and assess, within the setting of disability analysis.

Objectives

By the end of this section you will have refreshed your knowledge of:

Prolapsed intervertebral disc / sciatica

Cervical spondylosis

Peripheral neuropathy

Focal nerve compression syndromes

Raynaud’s Phenomenon, Hand-Arm Vibration Syndrome and Vibration White Finger

Duration


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Prolapsed Intervertebral Disc and Sciatica

Before you read this, you may wish to review the section on ‘Low Back Pain’ within the Evidence Based Protocols for the Disability Analyst (Issue 2 of the EBP CD was sent out earlier this year; recent starters will have received a copy at their initial training. The protocols can also be accessed on Livelink).

Cause

The spine is made up of vertebrae enclosing the vertebral (spinal) canal, which is occupied by the spinal cord. In between the vertebrae are intervertebral discs. They allow movement between the vertebral bodies and also function as shock absorbers.

Intervertebral discs are composed of a tough fibrous outer coating; annulus fibrosis and an inner gel like substance; nucleus pulposis.

A prolapsed intervertebral disc is caused by protrusion of the nucleus pulposis leading to impingement of adjacent nerve roots and nerves. However, even in tears that don’t cause protrusion, there may be similar symptoms – this is because inflammatory mediators are released, which may lead to local swelling which also results in impingement.

It often occurs suddenly in association with bending or lifting heavy weights. However, there is almost always underlying disc degeneration which is associated with normal ‘wear and tear’. Degeneration of the disc often begins to be seen in the 3rd decade and is often asymptomatic.

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You may see the term prolapsed intervertebral disc being shortened to PID. This is to be discouraged since it is confusing as other terms are also shortened to this acronym (including pelvic inflammatory disease).

Prolapsed intervertebral discs most commonly occur in the cervical and lumbar regions of the spine. They may be central or lateral.

A central disc prolapse occurs into the central spinal canal, compressing the spinal cord in the cervical region and cauda equina in the lumbar region. Compression of the cauda equina causes bilateral leg weakness often with severe bilateral sciatic pain, reduced sacral sensation and altered bladder control. This is a neurosurgical emergency requiring urgent MRI for diagnosis and urgent neurosurgical decompression.

A lateral disc prolapse will affect the nerve roots entering and leaving the intervertebral foramen. Lateral disc prolapse most commonly affect the L5/S1 disc (compressing the S1 root) or the L4/L5 disc (compressing the L5 root). Less often the C5/C6 (compressing the C6 root) and C6/C7 (compressing the C7 root) are affected. A prolapsed disc can be confirmed by MRI scan.

You may see references to the term spinal stenosis. Spinal stenosis is caused by a combination of a protruding intervertebral disc, spondylolisthesis (slippage between adjacent vertebrae), hypertrophy of intraspinal ligaments and spondylitic protrusions from vertebral bones leading to narrowing of the vertebral canal.

It is characterised by numbness, discomfort and weakness of the legs, which develop whilst walking, or during prolonged standing. The symptoms do not occur when exercising with spine flexed, such as in cycling. They are relieved by sitting down. There may be intermittent cauda equina compression with pain and altered bladder control. Again it can be confirmed on MRI scan. Treatment is usually surgery (laminectomy) often with good results.

Symptoms and Signs

A prolapsed intervertebral disc may be associated with local pain, produced by the annular tear and protective lumbar muscle spasm, with restriction of spinal movement. There may be loss of the normal lumbar lordosis due to muscle spasm. Impulse symptoms are common, where sneezing or coughing causes a worsening of the pain.

Sciatica is severe pain beginning in the lumbar region and radiating down the back of the leg to the knee, ankle or foot, depending on what nerve root is involved. It is exacerbated by stretching the nerve. Straight leg raising may be restricted, with pain radiating down the leg. True sciatic pain on straight leg raising will be reduced by bending the knee and exacerbated by dorsiflexing the foot. Remember that testing straight leg raising in our assessments should never involve you passively moving the leg.

Neurological disturbance, if present, is dependent on the level of the prolapsed disc. There may be focal muscle wasting, focal sensory impairment or loss and diminished or absent reflexes.

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Treatment

The majority of people with symptoms from a prolapsed disc will get better with conservative treatment such as pain relief and initial rest. Anti-inflammatory medication, physiotherapy, and muscle relaxants may also help. Whilst rest may initially be of benefit, current opinion is that prolonged rest is of no benefit and may in fact be detrimental.

Epidural treatment, where local anaesthetic or steroids are injected around the nerve roots, may help.

If the symptoms do not improve or there are significant neurological symptoms and signs, surgery may be required. Surgical treatment includes laminectomy, discectomy and microdiscectomy.

Surgery often relieves the pain immediately, but the neurological symptoms and signs, such as numbness and weakness, can take longer to improve and may not return completely to normal. There is a risk of recurrence.

Functional impact

There may be no functional impact.

The pain associated with the prolapsed disc may lead to restrictions of sitting, standing, walking, heavy lifting (of objects from the floor) and bending.

Where there is neurological involvement any associated impairment will depend on the site of the prolapsed disc. Examples include:

Foot drop (L5 root) may cause the claimant to catch their toe whilst walking.

Plantar reflex weakness (S1 root) may take the spring out of the claimant’s stride causing problems with walking.

Weak elbow extension (C7 root) may make it difficult to push open doors or find 3rd gear whilst driving.

Weak elbow flexion (C6 root) may make it difficult to lift objects.

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Consider the following examples. Think about what you have learnt in the neuroanatomy section.

Interaction: A claimant says that have a L4/5 disc prolapse. What symptoms might they have?

Interaction: What signs would be expected on examination?

Interaction: Consider a claimant with a L5/S1 disc prolapse. What symptoms might they complain of?

Interaction: What signs would be expected on examination?

Now re-review the information you have read thus far in Section Three, to check whether you have responded correctly.

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Cervical Spondylosis

Before you read this, you may wish to review the section on ‘Neck Pain’ within the

Evidence Based Protocols for the Disability Analyst (Available on CD, which you may have received at initial training, and which is also available on Livelink).

Cause

Cervical spondylosis is a degenerative condition, also known as cervical osteoarthritis, although the term is sometimes inappropriately applied to all non specific neck pain. With increasing age the cervical intervertebral discs shrink, becoming tougher and less flexible. This is associated with the growth of small bony spurs (osteophytes) and degenerative changes of the posterior facet joints. Cervical spondylosis tends to be most marked at C4/5, C5/6 and C6/7.

Cervical spondylosis may be associated with a nerve root compression or myelopathy.

Cervical nerve root compression may lead to dysfunction of that nerve root. You may see this sometimes referred to as cervical radiculopathy. C7 (60%) and C6 (25%) are the most commonly affected in nerve root compression.

A myelopathy relates to a problem with the spinal cord. Cervical myelopathy is compression of the spinal cord in the neck. Single or multiple levels of the spinal cord may be compressed between 3rd and 7th cervical vertebra. It is an uncommon complication.

You may see the term spondylitic radiculo-myelopathy, this simply means there is both myelopathy and nerve root compression.

About 50% of the population develop cervical spondylosis by the age of 50, increasing to 70% by the age of 60. It affects men and women equally but men tend to develop it earlier. As many asymptomatic people over the age of 30 show similar changes in x-rays, the boundary of normal aging and disease is difficult to delineate. A previous neck injury can pre-dispose to the development of cervical spondylosis.

The diagnosis of cervical spondylosis is made on clinical grounds alone, cervical x-rays can show degenerative changes but as these can be found in asymptomatic people, the changes correlate poorly with symptoms. An MRI scan is usually performed when neurological pathology is suspected.

Symptoms and Signs

Cervical spondylosis is associated with neck stiffness and pain worsened by movement. The pain may radiate to the base of skull, shoulders, arms hands and fingers. There may also be complaints of retro-orbital (behind the eye) or temporal pain, dizziness, poor balance and rarely syncope, or triggering of migraine.

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Neurological signs may be the initial presenting feature or may develop in already established disease.

Symptoms of nerve root compression may occur after some unusual strain or may occur spontaneously and usually come on over a few days. There may be complaints of pain, numbness, tingling or weakness in upper limbs.

Symptoms of cervical myelopathy depend on the level of compression:

Higher compressive neuropathy (C3-C5) can cause a syndrome of clumsy and numb hands with difficulty writing, loss of manual dexterity, diffuse non-specific weakness and abnormal sensations.

Lower compressive neuropathy (C6-C7) usually presents with weakness, stiffness and proprioceptive loss in the legs. There are often signs of spasticity. Urinary control may be affected, although urinary incontinence is rare. Urinary urgency, frequency or hesitancy may be reported.

Examination may show poorly localised tenderness and loss of cervical movement.

There may be signs of nerve root compression (which may be poorly localized). Pain is often complained of proximally whilst paraesthesiae occurs distally.

With cervical myelopathy there will be signs of upper motor neuron dysfunction:

Hyperactive deep tendon reflexes

Spasticity of upper limbs +/- spastic gait

Extensor (up-going) plantar reflex

Un-coordinated limbs

There may be wasting in triceps and intrinsic hand muscles (wasting of the intrinsic muscles of the hand is classic finding). Proximal muscle weakness is common, distal weakness is less common.

Loss of vibration sense and proprioception can occur in extremities, especially the feet.

Treatment

Treatment of cervical spondylosis is usually conservative including NSAIDS, physiotherapy and lifestyle modifications.

Cervical nerve root entrapment symptoms often resolve with conservative measures (in up to 75% of cases). Surgery is generally advised for cervical nerve root entrapment where there is intractable pain, progressive symptoms or weakness that fails to improve with conservative treatment.

Surgical treatment for cervical myelopathy remains controversial; but is generally recommended for moderate to severe myelopathy. Mechanical relief of cord

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compression does not always lead to improvement, because ischaemia of the cord is thought to be a compounding factor.

Functional impact

There may be no functional impairment.

Pain in the neck alone does not commonly produce significant loss of function in upper limbs. Lifting and carrying should not be affected by neck pain alone.

Where there is a neurological deficit, it may be associated with some loss of function.

C6/7 nerve root compression may affect reaching (but not lifting) and sensory impairment of index and middle fingers may affect pinch grip function

Myelopathy with cord compression at C3-5 may cause a problem with manual dexterity. Compression of spinal cord at a lower level C5-8 may affect gait and walking.

Consider the following example: A claimant tells you they have cervical spondylosis

Interaction: What symptoms might they complain of?

You noticed that on walking to the examination room, their gait was abnormal

Interaction: What specific neurological examination would you perform?


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Peripheral Neuropathy

Peripheral neuropathies can be broadly divided into two groups: generalised, and focal. In generalised peripheral neuropathy all nerve fibres are affected equally, irrespective of the peripheral nerve from which they are derived, leading to a generalised and symmetrical abnormality. Focal peripheral neuropathy affects individual peripheral nerves either singularly or in multiples, therefore signs and symptoms are restricted to the territory of the affected nerves. This section deals with generalised neuropathy. Focal peripheral neuropathies will be addressed in the following section.

Cause

Generalised peripheral neuropathy can either be due to axonal degeneration of the nerve fibres or demyelination of the nerve fibres.

Axonal degeneration affects all axons (both myelinated and unmyelinated). With regard to the sensory neurons; joint position, vibration sense, pain, light touch, pinprick and temperature sensation are all affected. The degeneration of the nerve fibres can result in denervation of muscles supplied by these nerves, resulting in weakness and wasting. The longest axons to the feet are affected first and most severely.

Demyelinating peripheral neuropathy only affects myelinated neurons. It causes impairment of joint position and vibration (however temperature and pinprick sensation normally remain intact). It usually causes more severe muscle weakness, including proximal muscles, because proximal nerve segments (sometimes including nerve roots) are affected. There is muscle weakness because of blockage of impulse conduction at demyelinated portion of nerve. However muscle wasting is less because the nerve fibres remain in continuity with the muscle.

There are multiple causes of generalized peripheral neuropathy. The most common causes that you will see in your role as a disability analyst are diabetes and alcohol misuse.

Diabetes

Diabetic peripheral neuropathy involves both axonal degeneration and demyelination. It is a complication of diabetes, although it occurs relatively early in the course of the disease. It is most often seen where there is poor diabetic control. It is common, affecting around 30% of people with diabetes.

It can affect sensory, motor and autonomic nerves. Most commonly seen is a symmetrical sensory peripheral neuropathy. It causes paraesthesiae and numbness, mainly in the feet, although it can also affect the hands. Neuropathic pain in the lower limbs is often reported (aching/piercing, worse at night, felt in the anterior aspect of the legs), as are burning sensations in the soles of the feet. There is often hyperaesthesia.

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On examination absent tendon reflexes and decreased vibration sense are early signs. There is often “glove and stocking” impairment of all modalities of sensation. There may be an abnormal wide-based gait. In advanced cases there may be muscle weakness and wasting.

People with diabetes may less commonly develop a motor diabetic neuropathy (also known as diabetic amyotrophy). This is generally an asymmetrical peripheral neuropathy. It presents as severe and progressive weakness and wasting of the proximal muscles of mainly the lower limb (although it can occur in upper limb as well). Often there is severe pain felt on the anterior aspect of the leg. Paraesthesia and hyperaesthesia are common. It may be associated with a significant loss of weight. It is thought to result from acute infarction of the lower motor neurons of the lumbosacral plexus. Management is supportive and recovery usually occurs over 12 months.

Diabetics are susceptible to a wide range of mononeuropathies affecting peripheral or cranial nerves. Nerves vulnerable to compression are most commonly affected, such as the median nerve in the carpal tunnel (see under ‘Nerve Compression Syndromes/ Focal Neuropathy’ below, for further examples).

Painful oculomotor (3rd) nerve palsies, often sparing the pupil, are common in older diabetics and resolve spontaneously. They cause frontal/periorbital pain and then diplopia. The parasympathetic nerve fibres within the 3rd cranial nerve that influence pupillary size, are found on the periphery of the nerve (when viewed cross-sectionally), thus making them less susceptible to ischemic damage (as they are closer to the vascular supply).

It is likely that pre-existing diabetic microvascular disease makes nerves unusually vulnerable to compression - these mononeuropathies may improve spontaneously, or with surgical decompression if appropriate. However, permanent residual abnormalities are common. Mononeuropathies of the thoracic or lumbar spinal nerves can also occur, leading to painful syndromes that mimic myocardial infarction, cholecystitis or appendicitis.

Alcohol misuse

Peripheral neuropathy occurs in up to 15 percent of people with chronic alcohol misuse. It is probably due to a combination of thiamine deficiency and direct toxic effects of ethanol.

It causes bilateral numbness and paraesthesiae, which is more pronounced distally. It is also associated with neuropathic pain, which may be severe.

Treatment is abstinence with thiamine replacement. Thiamine replacement may lead to some improvement in the condition. Specific treatment may be required for the painful neuropathy.

There are many other causes of peripheral neuropathy. Guillain-Barré syndrome is an example of a demyelinating peripheral neuropathy. Vincristine, Cisplatin, Isoniazid, Nitrofurantoin are examples of drugs that can cause peripheral neuropathies. Glue solvents, arsenic, lead, mercury, thallium and organophosphates

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are examples of chemically induced peripheral neuropathies. Some genetic conditions which cause peripheral neuropathies include Charcot-Marie-Tooth disease or hereditary sensory or motor neuropathy. Renal failure, liver failure and vitamin deficiencies, such as B12 and E are also causes.

Symptoms and Signs

Peripheral neuropathy generally begins with tingling or numbness in feet and fingers. The claimant may complain of weakness and clumsiness.

Examination often shows loss of pinprick and touch sensation in a ‘glove and stocking’ distribution.

Sensory loss in ‘glove and stocking’ pattern of distribution

There may be impaired joint position sensation on direct testing, with finger-nose ataxia, an abnormal heel-shin test and a positive Romberg’s sign. There may be weakness and wasting of muscles.

Tendon reflexes are usually lost in the affected area.

Nerve conduction tests will confirm the presence of a peripheral neuropathy.

Charcot joints may be present. These are joints that have been damaged because the claimant is unable to feel pain, leading to progressive destruction bone and joint. Most commonly affected joints are the knee and ankle.

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Treatment

Treatment involves treating the cause of the peripheral neuropathy. Where there are metabolic abnormalities or toxic causes, they should be corrected or removed. Where there is another cause, for example a genetic disorder, no specific treatment is available and management is supportive only.

Peripheral nerves do have some ability to regenerate. The amount of recovery depends on the severity of the neuropathy and the distance over which regeneration is required. Unfortunately with axonal degeneration it rarely recovers well even if the cause is removed. In peripheral neuropathies where the cause is demyelination, with treatment of the cause, there is likely to be a good recovery over weeks to months.

Functional impact

The claimant may describe difficulty with activities that involve walking. They may also describe difficulties with activities involving manual dexterity and coordination. Neuropathic pain may impact on their sleep and on their concentration thereby affecting their ability to carry out daily living activities. They may also report falls.

Consider the following example: A claimant with alcohol misuse tells you that they have fallen several times recently

Interaction: What would you ask about the history of their condition?

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Interaction: What examination would you perform in this case? What might you expect to find on examination?


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Nerve Compression Syndromes and Focal Neuropathy

Focal neuropathy reflects a lesion of an individual peripheral nerve. Causes of focal peripheral neuropathy include:

Compression

Trauma / Laceration

Vasculitis, causing ischaemic damage

Irradiation

Nerve sheath tumours

Tumour infiltration

Diabetes

Regeneration of a transected nerve can occur if the ends of the neural sheath are opposed. However it occurs very slowly and is often incomplete. Recovery time following compression will depend on the degree of damage to the nerve fibres.

The following conditions are the most common focal nerve neuropathies that we see:

Median nerve (carpal tunnel syndrome)

Carpal tunnel syndrome is the commonest peripheral nerve problem in UK. It results from compression of the median nerve as it passes under the transverse carpal ligament (flexor retinaculum) at the wrist.

Anatomy of the carpal tunnel

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There is increased pressure within the carpal tunnel, impairing the blood supply of the nerve, causing demyelination of axons eventually resulting in axonal loss. Pressure is increased by wrist flexion and extension and finger flexion. There is a strong genetic predisposition, other risk factors are pregnancy and obesity. Middle-aged women are most commonly affected. It can be associated with hypothyroidism, acromegaly, Cushing’s disease, rheumatoid arthritis, and repetitive use of vibrating tools.

Symptoms and Signs

Symptoms of carpal tunnel syndrome include painful tingling in thumb, index, middle and ring fingers. However claimants may find it difficult to correctly identify which fingers are involved. The symptoms classically occur at night and may wake the claimant up. They are also provoked by manual tasks such as writing and sewing. They may describe weakness or clumsiness of the hand. Claimants often describe improvement in the symptoms by changing hand posture or by shaking the hand.

There are often no physical signs when the claimant is examined. There may be sensory loss in median nerve distribution (lateral palm and thumb, index middle and lateral half of ring finger).

Skin area supplied by median nerve in the hand

The exact demarcation however is variable and the whole ring finger may be supplied by the median nerve.

Weakness and wasting of abductor brevis muscle (thenar eminence – ball of thumb) only occurs in advanced cases. In this situation there will be weakness of thumb opposition.

A positive Tinel’s sign may be found in carpal tunnel syndrome. The median nerve is tapped repetitively just proximal to the distal radius. If positive, tingling is felt in the appropriate median nerve distribution.

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A positive Phalen’s test may be found in carpal tunnel syndrome. This test is performed with the elbow resting on the desk and the forearm vertical. The wrist is then flexed with it being actively held (by the claimant) in that position. Another way would be asking the claimant to place the backs of both hands together to form right angles and hold the position. The test is considered positive if tingling or numbness is felt in the appropriate median nerve distribution within 60 seconds.

However neither test is particularly sensitive nor specific for carpal tunnel syndrome. Both tests are less reliable in advanced disease. Nerve conduction studies are recommended when the diagnosis is uncertain but do have a small false negative rate.

The median nerve can be transected or compressed at a more proximal level than the wrist, although this is less common. If it is affected at the shoulder or elbow, in addition to the above symptoms and signs, there may be pain in the forearm, medial (ulnar) deviation of the wrist when it is extended (due to paralysis of the lateral (radial) wrist flexor), inability to flex the terminal phalanx of the thumb and index finger, as well as some weakness of flexion of the terminal phalanx of the remaining fingers.

Treatment

Treatment involves addressing any known contributory causes. For claimants with mild to moderate symptoms the condition may be managed conservatively with splinting of the wrists at night, activity modification and steroid injection at the wrist.

The definitive treatment is surgical release of the carpal ligament to decompress the carpal tunnel. Surgery is generally offered to those in whom conservative measures have failed or those who present with severe disease, and is generally very successful.

Functional impact


The claimant may describe difficulty handling small objects. There may be difficulty with writing or performing repetitive manual dexterity tasks, or tasks where there are sustained hand or arm positions.

Ulnar Nerve

The nerve runs behind the humerus at the elbow. It is at this site where it can be damaged (by fracture/dislocation or trauma) or compressed.

The ulnar nerve supplies muscles that have the following actions; flexion of the wrist (medial (ulnar) side), flexion of little fingers at interphalangeal joint and metacarpophalangeal joint, partial flexion of ring finger, abduction of little finger, abduction and adduction of fingers, extension of terminal phalanges of fingers.

It supplies the skin of the medial palm, little finger and the medial half of the ring finger.

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Skin area supplied by ulnar nerve in the hand

Symptoms and Signs

Tingling, numbness and pain in the little and ring fingers and medial (ulnar) border of hand are the earliest symptoms. Over time weakness and wasting of the muscles supplied by the ulnar nerve will develop.

Examination may demonstrate sensory loss in the medial palm, little finger and medial ring finger. There may be weakness and wasting of the small hand muscles.

Longstanding ulnar nerve neuropathy results in a ‘claw hand’ where there is hyperextension at the metacarpophalangeal joints and flexion at the interphalangeal joints.

Treatment

Treatment for ulnar nerve compression may involve splinting of the elbow, surgery to decompress the cubital tunnel or transpose the nerve anteriorly.

Functional impact


The claimant may describe difficulty handling small objects and difficulty with tasks that require manual dexterity.

Radial Nerve

The radial nerve supplies the triceps muscle, which extends the elbow, and muscles that extend the wrist and the fingers.

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Most radial nerve neuropathies are due to compression. It can be precipitated by sleeping in abnormal position, often when intoxicated, with the arm over the back of a chair (known as 'Saturday night palsy'). In the past it was seen with use of “under the shoulder” crutches which lead to compression of the nerve in the axilla, however with the use of elbow crutches this is seen less often nowadays. It may also be seen after surgery when the anaesthetised patient’s arm is allowed to hang over the edge of the operating theatre table. Its course winds around the shaft of the humerus, where it is vulnerable to damage by humeral fracture, and rarely it can be damaged by dislocation of the elbow.

Symptoms and Signs

The principle findings are of weakness of finger and wrist extension and a small area of sensory loss on the dorsum of the thumb. The clinical features of radial nerve neuropathy depend upon the site of the injury.

Lesions in or above the axilla result in paresis and wasting of all the muscles supplied by the radial nerve. Clinically, this is manifest as weakness of forearm extension and flexion, wrist drop and finger drop, weakness of the long thumb abductor and extensor muscles and sensory loss on the dorsum of hand and forearm.

Skin area supplied by radial nerve in the hand

Lesions around the humerus often do not affect the extension of the elbow and may also spare wrist extension.

Lesions around the elbow lead to weakness of finger extension, and of thumb extension and abduction. There is little or no wrist drop, and usually, no sensory loss.

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Treatment

Treatment is usually supportive, allowing the nerve time to recover over weeks or months. Splinting of the wrist to assist wrist drop may improve function.

Functional impact


Depending of the level of the lesion, the claimant may have difficulty with lifting, and tasks requiring manual dexterity.

Common Peroneal Nerve

The common peroneal nerve is a branch of the sciatic nerve. It supplies the muscles that dorsiflex the feet and toes and everts the foot.

It is often damaged where it crosses the fibular head. There may be compression where the nerve passes over head of the fibula (lateral to and just below the knee) or it may be damaged by fractures or penetrating wounds at the upper end of the fibula. A plaster or splint can cause compression at this site.

Symptoms and Signs

The claimant may have foot drop and sensory loss over dorsum of foot and lateral shin.

Skin area supplied by common peroneal nerve

Treatment

If the cause is compression, with appropriate treatment, recovery is possible over weeks to months.

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Functional Impact

The claimant may describe difficulty with activities that involve walking and climbing stairs. The use of an appropriate splint will improve function significantly even in the presence of severe foot drop.

Lateral Cutaneous Nerve of the Thigh

This nerve carries sensation from the antero-lateral aspect of the thigh. The nerve may be compressed as it passes through the inguinal ligament just medial to the anterior superior iliac spine. This is also known as meralgia paraesthetica.

Symptoms and Signs

Compression of the nerve leads to tingling, paraesthesia or pain over the lateral border of the thigh. On examination there is sensory loss over the lateral border of the thigh. There is no related weakness.

Skin area supplied by lateral cutaneous nerve of thigh

Treatment

It may resolve spontaneously. Injection of local anaesthetic around the site of entrapment may help. If conservative measures fail surgical decompression of the nerve may be indicated.

Functional Impact

There is often no functional impact. It may rarely cause severe intractable chronic pain, with associated affects on day-to-day activity.

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Brachial Plexus Injuries

The brachial plexus is formed from the following spinal nerves: C5, C6, C7, C8 and T1 (C4 and T2 may occasionally contribute as well). Within the brachial plexus, the spinal nerves are redistributed into peripheral nerves supplying the upper limb. The brachial plexus is located in the neck and axilla bilaterally. Traumatic injury can occur with gunshot and stab wounds. However, it is most commonly injured in road traffic accidents, specifically motorbike accidents, when the nerves of the plexus are forcibly stretched. Damage to the brachial plexus can also occur during birth when shoulder dystocia (when the shoulder has difficulty passing through pelvis) is present.

Symptoms and signs

The symptoms and signs will depend on which parts of the plexus are involved. It is rare to have total plexus paralysis. The two most common types of injury are as follows:

Upper plexus paralysis, also known as Erb-Duchenne paralysis, occurs when a branch of the C5 spinal nerve, and sometimes the C6 spinal nerve as well, is damaged or torn. It occurs after the head is violently forced to one side, such as in a motorbike accident or birth trauma. Shoulder abduction and external rotation and elbow flexion are lost. In long standing lesions, the position of the limb is characteristic, known as the waiter’s tip deformity. The shoulder is internally rotated and the arm hangs at the side, with elbow extended and the wrist flexed and pronated and the fingers flexed. There is wasting of the paralysed muscles. The biceps reflex, and possibly the supinator reflex, is lost. There is usually no sensory loss.

Lower plexus paralysis, also known as Dejerine-Klumpke paralysis, occurs when the T1 spinal nerve, and rarely the C8 spinal nerve as well, is damaged or torn. It can occur after the forcible abduction of the arm or birth injury. Finger abduction and adduction is lost along with flexion at the MCP joints. In long standing lesions there is paralysis and wasting of the intrinsic muscles of the hand, resulting in a claw hand. There is usually sensory loss along the ulnar (medial) border of the hand and a variable distance up the forearm.

Treatment

Treatment of brachial plexus injuries is usually conservative and supportive. Recovery depends on the cause and severity of the injury. There may be little or no recovery. Brachial plexus lesions resulting from birth injury usually recover spontaneously over several months.

Functional impact

Depending on the site of the lesion, claimants may describe difficulty with tasks requiring lifting, reaching, and manual dexterity.

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Thoracic Outlet Syndrome

A thoracic outlet syndrome (TOS) is caused by compression of the brachial plexus and brachial vessels as they pass from the neck to the arm. It can produce a mixture of nerve compression symptoms and circulation changes in the arm and shoulder. Women are more prone to developing symptoms than men, in middle age.

The most common causes are costo-clavicular syndrome and cervical rib syndrome. Costo-clavicular syndrome occurs when the space between the collar bone (clavicle) and first rib is narrowed. This can be due to a congenital abnormality, or due to poor posture with rounded shoulders. Cervical rib syndrome occurs when there is an extra rib or tight fibrous band connecting the 7th cervical vertebra with the sternum. There is compression of the brachial plexus as it passes over this structure, often when the arm and shoulder are placed in certain positions. Symptoms are often due to compression of the 8th cervical and 1st thoracic parts of the plexus, with symptoms involving the inner arm down to the little finger.

Adson’s sign (a loss of a palpable radial pulse on the affected side) may be evident when the head is turned to the ipsilateral side, and chin slightly elevated, during deep inspiration. Although it was previously thought to be a reliable indicator of TOC, there is little evidence of inter-examiner reliability and many people without TOS will show a positive Adson’s sign. MRI scanning is the most useful investigation for revealing anatomical abnormalities.

Symptoms and Signs

In slim patients, the cervical rib may be able to be felt just above the collar bone.

Claimants will often complain of tingling or paraesthesiae down the medial arm to the little finger. It is often associated with pain, especially radiating to the medial border of the hand and forearm. Typically, the pain will be increased by raising the hand above the head. Examination may demonstrate sensory abnormalities in the C8 and/or T1 dermatome distribution. There may be weakness and wasting of the small muscles of the hand. However, the findings may differ depending on what part of the brachial plexus is compressed.

There may be vascular changes including changes in colour (blotchiness and cyanosis) and abnormal sweating in the affected limb.

Treatment

Surgery may be required to remove a cervical rib, fibrous band, or part of the first rib.

Functional Impact

There may be no functional impairment. Claimants may describe problems with tasks requiring manual dexterity.

Consider the following examples:

http://www.painclinic.org/home-mriscans.htm

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A claimant reports tingling in her hands

Interaction: What should you ask about in the “history of condition” section?

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Interaction: What examination would you perform?


A claimant reports a history of a dislocation of the elbow, complicated by ulnar nerve damage, which causes her a lot of problems:

Interaction: What tasks would you ask about in the typical day history that might reflect functional impairment?

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Interaction: What specifically needs to be examined in this case?


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Raynaud’s phenomenon, Hand-Arm Vibration Syndrome and Vibration White Finger

Raynaud’s phenomenon

Raynaud's Phenomenon (RP) is triggered by intense vasospasm of the peripheral arteries, usually on exposure to cold. It can be caused by:

Primary Raynaud’s Disease: constitutional, or idiopathic, white finger - the aetiology of which is unknown. It often affects other family members.

Secondary Raynaud’s Phenomenon: aetiology of this includes connective tissue disorders (e.g. Scleroderma), trauma to the extremities or to proximal blood vessels, vascular disease and vibration (e.g. Vibration White Finger)

RP affects approximately 5% of the population. It is more common in women than men (5:1). Most cases are due to Primary Raynaud’s Disease. The onset of Raynaud’s Disease and Reynaud’s Phenomenon is gradual (over a number of years), initially with attacks being rare and in winter only.

In the vast majority of cases the fingers are affected, (but it can affect the toes and, more rarely, the nose, ears, cheeks and chin), beginning with tingling and/or numbness in the tips of the fingers. As it progresses, blanching on exposure to intense cold develops, at first in the tips of the fingers, but over time it progresses to affect more and more of the finger, and to occur throughout the year, including summer.

The colour changes of RP are characteristic. The blanching is an intense whiteness with a well-defined demarcation and is circumferential. The blanching may last a few minutes or last up to an hour or two. Sometimes immersion in warm water speeds up recovery. On recovery the fingers may become cyanotic (i.e. turn a greyish–blue colour) or become hyperaemic (i.e. very red in colour). In severe cases, with the passage of time, there may be trophic changes of the fingers.

The ‘gold standard’ for diagnosing Raynaud’s Phenomenon is the clinical history given by the claimant. As the symptoms are intermittent, and only occur in cold conditions, it is rare to see an episode in an assessment setting.

Treatment includes simple measures such as keeping affected parts warm (heated gloves etc) and stopping smoking. Medication such as nifedipine and angiotensin-blocking drugs can help by dilating the affected small blood vessels. More serious disease can require nerve blocks or intravenous infusion therapy with iloprost to dilate the affected blood vessels.

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Hand-Arm Vibration Syndrome (HAVS)

HAVS is a syndrome which develops secondary to the use of hand-held vibrating tools. It includes blanching of the fingers, peripheral nerve damage (sensorineural problems), and musculoskeletal problems in the hands and arms. Not all elements are required for the diagnosis of HAVS to be made.

There is no universal description of HAVS. The Department of Trade and Industry defines HAVS as ‘exposure to vibration causing peripheral circulatory disturbances that manifest as vibration induced white finger, peripheral neurological disturbances such as numbness, tingling and paraesthesia and musculoskeletal disturbances in the hand and the arm’.

Vibration White Finger (VWF)

VWF is an example of a secondary form of Raynaud’s Phenomenon. It is now recognised that vibration can affect the small sensory nerves of the fingers exposed to hand-held vibrating tools. The symptoms (tingling and numbness) arising from this damage usually pre-dates the onset of vascular symptoms, and may occur in the absence of vascular symptoms. For progression of condition there must be continued exposure of the hand to vibration.

Functional Impact

There may be no functional impact. The claimant may describe difficulty with tasks involving manual dexterity.

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Further Reading

If you would like to read more about the topics included in this document the following books provide more in-depth information:

Atos Healthcare EBM Protocols on Neck Pain [MED S2 CMEP~0049(b)]; and Low Back Pain [MED S2 CMEP~0049(a)] (available via Livelink for those HCPS with access, or via the Evidence Based Protocols CD, for those who do not have Livelink access)

Neuroanatomy, an Illustrated Colour Text. AR Crossman and D Neary; Churchill Livingstone

Brain’s Diseases of the Nervous System. M Donaghy; Oxford University Press

Neurological Examination Made Easy. G Fuller; Churchill Livingstone

Neurology: An Illustrated Colour Text. G Fuller; Churchill Livingstone

Oxford Handbook of Neurology. H Manji et al; Oxford University Press

Harrison's Neurology in Clinical Medicine. SL Hauser et al; McGraw-Hill

Clinical Neuroanatomy Made Ridiculously Simple. S Goldberg

Crash Course: Neurology (Crash Course-UK). C Turner; Mosby

Neurology in Clinical Practice: Volume II The Neurological Disorders. WG Bradley, RB Daroff, GM Fenichel, and J Jankovic; Butterworth Heinemann

Textbook of Clinical Neurology. CG Goetz; Saunders

Orthopaedic Neurology: A Diagnostic Guide to Neurologic Levels. S Hoppenfeld; Lippincott, Williams, & Wilkins

http://www.amazon.co.uk/Neurology-Geraint-Fuller-FRCP-Dr/dp/0702032247/ref=sr_1_1?s=books&ie=UTF8&qid=1287505969&sr=1-1

http://www.amazon.co.uk/Oxford-Handbook-Neurology-Handbooks/dp/0198509731/ref=sr_1_8?s=books&ie=UTF8&qid=1287506165&sr=1-8

http://www.amazon.co.uk/Harrisons-Neurology-Clinical-Medicine-Stephen/dp/0071457453/ref=sr_1_22?s=books&ie=UTF8&qid=1287505793&sr=1-22

http://www.amazon.co.uk/Crash-Course-Neurology-Course-UK/dp/0723434697/ref=sr_1_4?s=books&ie=UTF8&qid=1287506061&sr=1-4

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Section Four – Multiple Choice Questionnaire

Welcome to the final section of your Learning Pack. This section is a multiple choice questionnaire (MCQ) exercise, which you should complete and forward to the Clinical Manager at your local Medical Service Centre (MSC).

Duration


Instructions

This is a true/false questionnaire, which means you are asked a series of questions and given a choice of a true or false response for each question. You should attempt all questions, ticking the answer you believe to be correct.

The completed MCQ must be returned to the Medial Manager at your local Medical Services Centre (MSC) for marking. The pass mark is 85% or above. The Clinical Manager will ask you to read the documents again and then repeat the MCQ, if you achieve less than 85%.

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Neurological Update MCQ

Name (Please Print):

Date:

GMC/NMC/HPC Number:

Signature:

Base (MSC):

MCQ: Neurological Update True False

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Glossary

Afferent neuron: neuron carrying signals towards the central nervous system

Annulus fibrosis: tough fibrous outer coating of an intervertebral disc

ANS: acronym for Autonomic Nervous System - the system of nerves that innervates and controls the blood vessels, heart, smooth muscles, internal organs, and glands. It consists of sympathetic and parasympathetic portions

Astrocyte: a type of cell found in nervous system

Ataxia: loss of coordination, especially in limbs

Axon: the part (or process) of the neuron that transmits signals away from cell body

Babinski sign: an abnormal plantar reflex (extensor or upward movement of big toe)

Brachial plexus: a network of nerves in neck and axilla, where spinal nerves are redistributed into peripheral nerves which supply the chest and upper limb

Brainstem: part of the brain, continuous with spinal cord, contains centres controlling vital functions including respiration, cardiovascular system and level of consciousness

Cauda equina: spinal nerve roots in vertebral canal below the level of the L1 vertebrae (where the spinal cord ends)

Cerebellum: part of the brain coordinating voluntary movements, posture, and balance

Cerebrum: the largest part of the brain, controlling and integrating motor, sensory, and higher mental functions, such as thought, reason, emotion, and memory. It is formed of two hemispheres

Charcot joint / Charcot arthropathy: disease of a joint where pain cannot be felt, leading to progressive destruction bone and joint

Chorea: involuntary abnormal movement

Clonus: repetitive, rapid contraction and relaxation of a muscle, occurring in succession, after forcible extension or flexion

CNS: acronym for Central Nervous System, which consists of the brain and spinal cord

Cogwheel rigidity: a type of increased tone, often seen in Parkinson’s disease

Decussation: a nerve or tract of nerve fibres that crosses from one side of the central nervous system to the other

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Demyelination: loss of myelin sheath of the neuron

Dendrites: the part (or process) of the neuron that transmits signals towards the cell body

Dermatome: area of skin supplied by one spinal nerve

Discectomy: surgery to remove part or all of an intervertebral disc

Distal: located away from the centre of the body. It is the opposite of proximal

Dorsal: pertaining to or situated at the back

Dorsiflexion: flexion in a dorsal direction, used to describe upwards flexion of the foot or toes; the opposite of this is plantarflexion

Dystonia: abnormal movement or posture resulting from prolonged muscle contraction

Efferent neuron: a neuron carrying signals away from the central nervous system

Eversion: movement of being turned or rotated outward, especially in the foot; the opposite of this is inversion

Extra-pyramidal tracts: relating to or involving neural pathways situated outside or independent of the pyramidal tracts. These are motor pathways that are beyond voluntary control. Their main function is to help control posture and muscle tone

Fasciculation: involuntary contractions of groups of muscle fibres

Ganglia: groups of nerve cell bodies outside the brain or spinal cord

Grey matter: concentrated groups of neuron cell bodies in the CNS

HAVS: acronym for Hand-Arm Vibration Syndrome

Hyperaesthesia: an abnormal increase in sensitivity to sensory stimuli

Hyperreflexia: increased or brisk reflexes

Hypertonia: increased tone

Hypertrophy: excessive enlargement of a part or organ (due to an increase in size of cells rather than increased numbers of cells)

Hyporeflexia: reduced reflexes

Hypotonia: decreased tone

Inversion: movement of being turned or rotated inward, especially in relation to the foot; the opposite of this is eversion

http://en.wikipedia.org/wiki/Muscle_tone

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Intervertebral foramen: opening that give passage to the spinal nerves from the vertebral canal, formed by the juxtaposition of the pedicles of adjacent vertebrae

Laminectomy: surgery to remove part of the vertebral bone (the lamina) to enlarge the spinal canal

Lateral: situated or extending away from the median plane of the body. It is the opposite of medial

Lead pipe rigidity: a type of increased tone

Lumbosacral plexus: a network of nerves where spinal nerves are redistributed into peripheral nerves which supply the pelvis, buttocks and lower limbs

Medial: situated in, or extending toward the median plane of the body. It is the opposite of lateral

Microdiscectomy: surgery to remove part of an intervertebral disc using a microscope

Microglial: a type of cell found in nervous system

Micturition: passing urine

Monosynaptic: having or involving a single neural synapse.

Motor unit: group of muscle cells supplied by one motor neuron

Myelin Sheath: a wrapping of myelin around certain nerve axons, that speeds up nerve impulses

Myelopathy: disorder of the spinal cord

Myoclonic jerk: a type of abnormal movement

Myoneural junction: junction between motor neuron and muscle cell

Myopathy: disorder of muscle tissue

Myotome: group of muscles supplied by a single nerve root

Nerve root: each segment of the spine gives off a ventral and dorsal nerve root bilaterally; these unite to form a spinal nerve

Neuron: nerve cell

Neuropathic pain: pain that has a neurological origin (the term neuralgia has been used in the past)

Neuropathy: a disorder of the nervous system

Neurotransmitter: chemical used to transmit impulses between nerve cells

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Nucleosis pulposus: inner gel-like substance of intervertebral disc

Oligodendrocyte: a type of cell found in nervous system

Osteophyte: small, abnormal bony outgrowth

Palsy: complete or partial muscle paralysis, often accompanied by loss of sensation

Paraesthesia: (pl. paraesthesiae) abnormal sensation such as prickling, tingling, itching or pins and needles

Parasympathetic nerve: component of autonomic nervous system.

Paresis: weak or partial paralysis of affected part

Phalen’s test: test used in examination of suspected carpal tunnel syndrome, where the wrist is flexed and actively held in that position

PID: acronym sometimes used to represent Prolapsed Intervertebral Disc; its use should be avoided as the abbreviation also represents Pelvic Inflammatory Disease!

Plantarflexion: movement of the foot that flexes the foot or toes downward toward the sole; the opposite of this is dorsiflexion

Plegia: complete paralysis of affected part

PNS: acronym used for Peripheral Nervous System, which consists of the cranial nerves and spinal nerves. The abbreviation should be avoided unless it is absolutely clear what is meant.

Polysynaptic: having or involving more than one synapse in the nervous system

Proprioception: unconscious perception of movement and spatial orientation arising from stimuli within the body itself

Proximal: located towards the centre of the body; and being the opposite of distal

Pyramidal tracts: tracts of descending motor fibres that are involved in voluntary movement (also known as corticospinal tracts)

Radiculopathy: pain caused by nerve root compression

Romberg’s sign: is a test of joint position sense

Sciatica: pain in the distribution of the sciatic nerve, generally extending down the back of the leg to the foot

Skeletal muscle: voluntary muscle tissue, connected at either or both extremities with a bone

Smooth muscle: involuntary muscle tissue in the walls of organs and blood vessels

Spasticity: increased tone

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Spondylolithesis: forward slippage of one vertebra on another

Spondylosis: degenerative disease of the spinal column, leading to fusion and immobilization of the vertebral bones

Sympathetic nerve: component of autonomic nervous system

Synapse: specialised junction between nerve cells where impulses are transmitted

Tardive dyskinesia: involuntary jerky movements of the face, tongue, jaws, trunk, and limbs

Tinel’s sign: test used in examination of suspected carpal tunnel syndrome, where the median nerve is tapped repetitively just proximal to the distal radius

Tract: a bundle of nerve fibres having a common origin and destination

Transected: completely divided

Tremor: abnormal involuntary movement

Trophic changes: changes resulting from interruption of nerve supply

Ventral: relating to or situated on or close to the anterior aspect of the human body

Vertebra: (pl. vertebrae) bones composing spinal column

VWF: acronym for Vibration White Finger

White matter: myelinated nerve fibres within the CNS

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Observation Form

Please photocopy this page and use it for any comments and observations on this document, its contents, or layout, or your experience of using it. If you are aware of other standards to which this document should refer, or a better standard, you are requested to indicate this on the form. Your comments will be taken into account at the next scheduled review.

Name of sender: ________________________ Date: _____________ Location and telephone number:____________________________________

Please return this form to: xxxxxxxxxxxxxxx Service Delivery Lead Atos Healthcare 3300 Solihull Parkway Birmingham Business Park Birmingham

B37 7YQ

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