Case 1 - Leah French (Stroke)

8/2/2019 Case 1 - Leah French (Stroke)

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BMB CASE #1 - LEAH FRENCH

The Doctor, Knowledge of Health and Illness

1 Review the basic organisation of the brain in terms of: hemispheres and lobes of the cortex; cerebellum; midbrain; pons; medulla oblongata; and

ventricles.

2 Describe how the cerebral blood flow is controlled and the importance of constant blood flow to brain cells.

3 Describe the major vessels of the cerebral circulation and the regions of the cerebral cortex supplied by the 3 main cerebral arteries.

4 Identify the main arteries of the vertebro-basilar circulation.

5 Describe the neural pathways involved in the control of voluntary movements mentioning the key anatomic landmarks related to these

pathways.

6 Describe the main somato-sensory pathways, mentioning the key anatomic landmarks related to these pathways.

7 Describe the structure, location and arrangement of fibre tracts and the blood supply of the internal capsule.

8 Identify the regions (primary, unimodal and multimodal association areas) of the cerebral cortex associated with voluntary movements, somatic

sensations and language, and briefly describe their functions.

9 Describe the anatomy of the cerebellum including the different functional regions.

10 Describe the role of the cerebellum in controlling limb movements.

11 Define upper and lower motor neurons and describe the clinical features of upper and lower motor neuron lesions.

12 Describe the main clinical features that differentiate occlusion of one of the 3 main cerebral arteries.

13 Describe and differentiate between the clinical features of unilateral spinal cord, brainstem, internal capsular and cortical lesions.

14 Describe the major subtypes of stroke (haemorrhagic, ischaemic, thromboembolic) and their pathological consequences.

15 Identify the major risk factors of cerebrovascular disease.

The Doctor, Law, Ethics and Professional Practice

16 Identify the principles of patient safety in health care organizations.

17 Discuss strategies to promote patient safety in the clinic.18 Identify the professional obligation to disclose medical harm and adverse events to patients, outlined in the Australian National Open Disclosure

Standard (2003).

19 Explain the ethical importance of acknowledging wrongdoing which has caused harm to a patient.

The Doctor and Patient

20 Demonstrate competence in exploring a patient's experience of sensory disturbance, muscle weakness or paralysis including:

the cardinal characteristics of the symptom and its time course

relevant associated symptoms

the patient's understanding of, and concerns about, what they are experiencing

21 Demonstrate competence in the physical examination of a patient for the assessment of radicular pain, sensory disturbance, muscle weakness,

paralysis or clumsiness in the lower limbs:

demonstrate appropriate infection control manoeuvres prior to and after examination of a patient [REVISION]

describe the anatomy of the major nerves of the lower limb and the muscle groups of the lower limb relevant to clinical examination

prepare a patient appropriately for neurological examination in relation to appropriate explanation, confirmation of consent and patient

positioning [REVISION] observe the lower limbs for muscle wasting, fasciculation or abnormal movements, comparing the two sides, then discuss the significance

of any abnormal findings

assess the tone of all muscle groups in the lower limbs, comparing the two sides, then discuss the significance of any abnormal findings

test the power of all muscle groups in the lower limbs, comparing the two sides, then discuss the significance of any abnormal findings

test the knee jerks, ankle jerks and plantar reflexes, comparing the two sides, then discuss the significance of any abnormal findings

test the sensation in the lower limbs through light touch and pin-prick, as well as position sense at the hallux, using appropriate techniques

and comparing the two sides, then discuss the significance of any abnormal findings

describe the dermatomes of the trunk and lower limb, as well as the sensory territories of the major nerves of the lower limb

recognise the common conditions affecting the nerves of the lower limb and discuss the historical and examination features characteristic

of each

22 Demonstrate competence in the physical examination of a patient for the assessment of radicular pain, sensory disturbance, muscle weakness,

paralysis or clumsiness in the upper limbs:

demonstrate appropriate infection control manoeuvres prior to and after examination of a patient [REVISION]

describe the anatomy of the major nerves of the upper limb and the muscle groups of the upper limb relevant to clinical examination observe the upper limbs for muscle wasting, fasciculation or abnormal movements, comparing the two sides, then discuss the significance

of any abnormal findings

assess the tone of all muscle groups in the upper limbs, comparing the two sides, then discuss the significance of any abnormal findings

test the power of all muscle groups in the upper limbs, comparing the two sides, then discuss the significance of any abnormal findings

test the biceps jerks, triceps jerks and supinator reflexes, comparing the two sides, then discuss the significance of any abnormal findings

test the sensation in the upper limbs through light touch and pin-prick, using appropriate techniques and comparing the two sides, then

discuss the significance of any abnormal findings

describe the dermatomes of the neck and upper limb, as well as the sensory territories of the major nerves of the upper limb

recognise the common conditions affecting the nerves of the upper limb and discuss the historical and examination features characteristic

of each

23 Demonstrate competence in exploring a patient's experience of dizziness, fits, faints or 'funny turns' including: the cardinal characteristics of the

symptom and its time course; relevant associated symptoms, and the patient's understanding of, and concerns about, what they are

experiencing. [REVISION]

The Doctor and Health in the Community

24 Describe the general principles of rehabilitation of the older patient with stroke.


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1. REVIEW THE BASIC ORGANISATION OF THE BRAIN IN TERMS OF: HEMISPHERES AND LOBES OF THE CORTEX;

CEREBELLUM; MIDBRAIN; PONS; MEDULLA OBLONGATA; AND VENTRICLES.

The dirty mess met my sponge

Fibres = PAC

BASICS

Forebrain

Telencephalon cerebrum

Diencephalon thalamus Relay and processing of sensory infohypothalamus Centre for controlling emotion, ANS and hormone production

midbrain Mesencephalon midbrain

Processing of visual and auditory data (colliculi)

Generation of reflexive somatic motor response ()

Consciousness (reticulospinal)

Hindbrain

Metencephalon pons and cerebellum

Myelencephalon - medulla

Medulla

Grey matter:

- Horns of spinal cord

- Cerebral cortex

- Basal ganglia

- Nuclei in SC and brainstem

Fibre Types:

- Commissural L to R (eg: CC)

- Projection brain to SC (eg: CSp)

- Association in a hemisphere (eg:uncinated fasciculus)

Fissures:

- Longtitudinal

- Transverse

Sulci

- Central

- Parietoocipital

- Lateral

Gyri


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BASAL GANGLIA

BG is a functional unit

- Putamen

- Globus pallidus

- Caudate

- Substanstia nigra

- Subthalamic nucleus

Striatum = caudate + putamen

- Major input place- Decision making, action selection and initiation

- In x-section they look separated (by IC)

Corpus striatum = caudate + putamen + globus striatum

Lentiform Nucleus = putamen + globus pallidus

- Separated from other basal ganglia by the internal

capsule


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CEREBELLUM

See LO9

BRAINSTEM

MIDBRAIN

PONS


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MEDULLA

VENTRICLES

INTERNAL CAPSULE see LO7


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2. DESCRIBE HOW THE CEREBRAL BLOOD FLOW IS CONTROLLED AND THE IMPORTANCE OF CONSTANT BLOOD FLOW TO

BRAIN CELLS.

4 main mechanisms control cerebral blood flow:

1. pressure autoregulation

poorly understood local vascular mechanism. This normally maintains constant blood flow btw 50-150mmHg. In

traumatised brain injury this mechanism is comprimised

2. metabolic autoregulationenergy metabolites cause local vasodilation

3. chemical factors

PCO2 causes local vasodilation. Hyperventilation can lead to a mean reduction in intracranial pressure of about 50% within

2-30 minutes. When PaCO2 < 25 mmHg there is no further reduction in CBF. Therefore there is no advantage in inducing

further hypocapnia as this will only shift the oxygen dissociation curve further to the right, making oxygen less available to

the tissues.

4. SNS determines MAP which influences cerebral vascular resistance but only minimally (5-10%)http://www.anaesthesiauk.com/article.aspx?articleid=100754

Importance:

- brain stores no energy + completely dependent upon blood glucose as substrate (during a fast brain can use ketones) only able to

withstand very short periods of ischaemia- Brain does not tolerate changes in chemical constituents well (ie too much N, too much neurotransmitter

- rises or drops CBF cause rises or drops in ICP

3. DESCRIBE THE MAJOR VESSELS OF THE CEREBRAL CIRCULATION AND THE REGIONS OF THE CEREBRAL CORTEX

SUPPLIED BY THE 3 MAIN CEREBRAL ARTERIES.
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ACA Longitudinal fissure and mainly runs on medial surface of brain

Pericallosal

Callosomarginal

- Medial precentral gyrus

- Medial postcentral gyrus

- medial frontal

- anterior4/5 of the corpus

callosum

- medial parietal

- medial orbital

- Anterior limb of the internal

capsule

- basal ganglia

MCA Lateral sulcus and onto the lateral surface of brain

M1 - from the termination of the ICA to the bi/trifurcation

M2 - the segment running in the lateral (Sylvian) fissure

M3

- coming out of the lateral fissure, also known as the operator

M4 - cortical portions.

lateral striate or

lenticulostriate

- lentiform Nu

- caudate

- internal capsule

Superior

division

- Pre and post central gyri

- Premotor AA

- supplemental motor AA

- Brocas area

- Posterior parietal AA

inferior division - Visual radiation

- Temporal lobe

- Posterior parietal AA

- 1 Auditory

- Wernickes area

- Visual cortex

PCA Around the cerebral peduncle into the transverse fissure on the base of

temporal and occipital lobes

CN 3 runs between PCA and sup cerebellar A

- Lateral geniculate body- Occipital cortex

- lentiform nucleus

- midbrain

- pineal

- medial geniculate bodies

- thalamus


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Venous Drainage

superior sagittal, inferior sagittal, straight, transverse, sigmoid, and occipital sinuses, the confluence of sinuses, and the cavernous,

sphenoparietal, superior petrosal, inferior petrosal and basilar sinuses drain into internal jugular.

Emmissionary veins drain the scalp into the sinus, they are a common route of infection.

Bridging veins from brain to sinus, break in subdural.

Cavernous sinus drains everything from face.


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4. IDENTIFY THE MAIN ARTERIES OF THE VERTEBRO-BASILAR CIRCULATION.

Internal Carotid

1. Bifurcation of CC

2. IC into cranium through carotid canal in temporal bone

3. Cavernous sinus

4. Circle of willis

Major branches

1. Ophthalmic

2. Posterior communicating3. Anterior choroidal

Vertebral Artery

1. Branches from subclavian

2. Travels through transverse foramina C1-C6

3. Foramen magnum

4. Up, forward and medial to medulla

5. Joins together in midline to form Basilar

Branches:

1. Meningeal supplies bone and dura of posterior cranial fossa

2. Post and ant spinal branches

3. Post inf cerebellar

4. Medullary branches (paramedian branches of VA)

Basilar Artery

1. Ascends in medial groove of pons2. At top of pons splits into 2 PCA

Branches

1. Ant inf cerebrallar A

2. Sup cerebellar A

3. Pontine branches

4. Labyrinthine long artery that travels with CNVIII to internal

ear

5. PCA

Cerebellar Circulation


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5. DESCRIBE THE NEURAL PATHWAYS INVOLVED IN THE CONTROL OF VOLUNTARY MOVEMENTS MENTIONING THE KEY

ANATOMIC LANDMARKS RELATED TO THESE PATHWAYS.

CSp = CR P limb IC CP basilar pons where theyre scattered amongst transverse pontine fibre medcullary pyramid D L and A CSp

CBulbar = same as above except mostly bilaterally innervated and synapse in brain stem Nu

Corticospinal Tract

Voluntary motor control of the limbs and trunk is

innervated via the corticospinal tract.

UMN originate from the

Primary motor cortex (50%)

Supplementary motor cortex

Premotor cortex

Primary Somatosensory cortex

Parietal lobe

Cingulated gyrus

They travel through corona radiata, down the

posterior limb of the IC, through the middle section

of the cerebral peduncle in the midbrain, through

the basilar pons where they are scattered among

the transverse pontine fibres and nuclei of thepontine grey matter. They come together again to

form the medullary pyramid

Some decussate and form the

contralateral lateral corticospinal tract

Some stay ipsilateral and form the

anterior corticospinal tract.

The anterior corticospinal tract innervates the axial

and proximal limb muscles whereas the lateral

corticospinal tract innervates the limbs.

The lateral corticospinal tract exits at the correct

level by synapsing in the ventral horn of the spinal

cord with the LMN (). The LMN travels out via theventral root, into the spinal nerve to innervate

skeletal muscle.

One LMN innervates one motor unit


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Corticobulbar Tract

Voluntary motor control of the face and neck

UMN originate from the

Primary motor cortex (50%)

They travel down the genu of the IC, through the

middle section of the ccan synapse on the CN

nuclei in the midbrain, pons and medulla

- CN III and IV in the midbrain

- CN V, VI, VII in the pons

- CN IX, X, XI, XII in the medulla

This tract innervates CN bilaterally except the

lower facial nuclei which are innervated only

unilaterally (below the eyes) and CNXII which is

unilateral as well

CN III, IV, VI may be more complex.


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Tectospinal tract

Originate from superior colliculus, cross in the

posterior tegmental decussation and distribute to

cervical levels

Superior colliculus receives input from lots of

areas but most organised is the visual cortex

Mainly influences trunk/facial motor reflexes in

relation to visual inputs. Ie turning away from

bright light, away from things flying toward your

head

travels with anterior CSp tract

Reticulospinal Tracts

Originates in the pontine and medullary reticular

Nu. Pontine is uncrossed and medullary project

bilaterally.

Projects to axial musculature

1. Integrates information from the motor

systems to coordinate automatic

movements of locomotion and posture.

2. Facilitates and inhibits voluntary

movement, influences muscle tone.3. Mediates autonomic functions

4. Modulates pain impulses

5. Influences blood flow to lateral

geniculate



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Rubrospinal Tract

Project from the red Nu, cross in the anterior

tegmental decussation and distribute to all spinal

levels (cervical much more though)

Red Nu receives input from upper extremity area

of the motor cortex, and also (much less though)

lower extremity motor cortex

Mainly influences limbs - UL flexion

travels with lateral CSp tract

Vestibulospinal Tract

Originate from the medial and lateral Vestibulo

Nu in the pons.

Medial project bilaterally

Lateral project ipsilateral and is a component of

the medial longitudinal fasciculus.

Mainly influences trunk - antigravity muscles.

These work involuntarily when your centre of

gravity changes to keep you from toppling over



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6. DESCRIBE THE MAIN SOMATO-SENSORY PATHWAYS, MENTIONING THE KEY ANATOMIC LANDMARKS RELATED TO

THESE PATHWAYS.

DCML = 1: skin CB in dorsal ganglion G/C fasciculus ventral horn 2: D up ML to VPL of thalamus 3: p limb IC to somatosensory

ALS = 1: skin CB in dorsal ganglion ventral horn 2: D obliquely and travels up ALS VPL of thalamus 3: p limb IC to somatosensory

Dorsal Column Medial Lemniscus (DCML)

1st

order neuron travels from the sensory area,

cell body in the dorsal ganglion enters the dorsal

horn to travel vertically in the gracilus/cuneatefasciculus until it reaches the gracilus/cuneate

Nu in the medulla. Here it synapses with a 2nd

order neuron.

2nd

order neuron decussates and travsels up the

dorsal column medial lemniscus on the opposite

side. Enters the VPL of the thalamus and

synapses with the 3rd

order neuron

3rd

order neuron travels via the posterior limb of

the IC to enter the 1 somatosensory cortex in

the post central gyrus.

This is responsible for

- Vibration

- Conscious proprioception

- Discriminative touch

- Pressure

- Two point discrimination

Damage to this pathway results in:

1. Loss of vibration sense

2. Loss of position sense

3. Loss of discriminative touch (tactile agnosia)

- agraphesthesia (writing on skin)

- astereognesia (object in hand)

stereoanaethesia


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Anteriolateral system

1st

order neuron from the area of sensation, cell

body in dorsal ganglion, enters the dorsal horn

and synapses with 2nd

order neuron.

2nd

order neuron decussates over several levels,

travels up through the anteriolateral system into

the medulla, pons and midbrain. They give off

branches to the reticular formation

(spinoreticular fibres), the midbrain (spinotectal

fibres to deep layers of superior colluculus,

spinoperiaqueductal fibres), the hypothalamus

(spinohypothalamic), accessory olivary Nu,

intralaminar Nu. They eventually synapse with

the 3rd

order neurons in the VPL of the thalamus.

3rd

order neurons travel from the VPL of the

thalamus up through posterior limb of the IC to

the somatosensory cortex in the post central

gyrus.

This is responsible for

- Pain

- Temperature- Crude touch

Damage to this pathway results in:

1. Loss of pain and temperature 2 levels below

lesion on contralateral side


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7. DESCRIBE THE STRUCTURE, LOCATION AND ARRANGEMENT OF FIBRE TRACTS AND THE BLOOD SUPPLY OF THE

INTERNAL CAPSULE.

Sublentiular = auditory radiation

Retrolenticular = optic radiation

8. IDENTIFY THE REGIONS (PRIMARY, UNIMODAL AND MULTIMODAL ASSOCIATION AREAS) OF THE CEREBRAL CORTEX

ASSOCIATED WITH VOLUNTARY MOVEMENTS, SOMATIC SENSATIONS AND L ANGUAGE, AND BRIEFLY DESCRIBE THEIR

FUNCTIONS.

Multimodal Association Areas:

A. Parieto-occipitotemporal Association Area

Analysis of spatial coordinate of the body - receives visual input +

somatosensory input

Wernickes area area for language comprehension

Angular gyrus - Area for initial processing of visual language

Area for naming objects auditory and visual input

B. Prefrontal Association Area

Receives input from parietooccipitotemporal AA

Important for motor planning, elaboration of thoughts, working memory

Output to ...

Brocas Area word formation

C. Limbic Association Area

Found in anterior pole of temporal lobe, ventral frontal lobe, cingulated

gyrus

Responsible for behaviour, emotions, motivation, emotional drive

Voluntary movements1 Motor cortex

> dedicate to controlling hands and muscles of speech

Excitation of one motor cortex neuron usually excites a specific muscle cf a specific

muscle

Premotor Area

Generates a pattern of mvmt. More important than supplementary motor area for

fine movement sequences. Sends signals to 1 motor cortex or to basal ganglia.

Includes: brocas area, voluntary eye mvmt, head rotation, hand mvmts.

Supplementary motor area

Elicits bilateral motor action. Body-wide movements, fixation movements of the

different segments of the body, positional

movements of the head and eyes, and so forth, as backgroundfor the finer motor control of the arms and hands by the premotor area and primary

motor cortex. Feedback mechanism of cerebellar influence in Motor

control


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Cerebellum

Responsible for:

- sequencing of motor activities

- Monitors and makes corrective adjustments in the motor activities while

they are being executed

- Learns from motor mistakes to make stronger or weaker output

corrections

Input:

- Motor plan via corticopontocerebellar pathway

- Sensory info from periphery via dorsal, ventral,

Output:

- instantaneous subconscious corrective signals are transmitted back into

the motor system to or the levels of activation of specific muscles

Important for: running, typing, talking.

Loss:

VANISH DDT = vertigo, ataxia, nystagmus, intention tremor, slurred

speech, hypotonia, dysdiadocokinesia, dysmetria, titubation

PINARDS = Past-pointing, intention tremor, nystagmus, ataxia, rebound, dysdiad,

slurred speech

Basal Ganglia

Responsible for: help to plan and control complex patterns of muscle mvmt, control

relative intensities of separate mvmts, direction of mvmts, sequencing multiple

successive and parallel mvmts for achieving complex motor goals.


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Somatic sensation

Language located in dominant hemisphere L side in 95%

Wernickes area (aka general interpretive area, tertiary association area, knowing area, Gnostic

area) receives input from the somatic, auditory and visual association areas of both hemispheres

via corpus callosum. Most important area for higher brain function/intelligence and interpreting

the complicated meanings of different patterns of sensory experienceWhen wernickes is destroyed person cannot perform mathematics, read, think through logical

problems. Non dominant side damage to same area decreases enjoyment of music, non verbal

visual experiences, spatial relations, body language, intonation in voice.

Angular Gyrus most inferior portion of posterior parietal lobe immediately behind wernickes area.

Vital for reading. A lesion in this area causes the blockage of visual input into wernickes area and

the symptoms of dyslexia (word blindness) where the person can see a word and know its a word

but not what it means.

Brocas area

Premotor speech area responsible for formation of words by exciting simultanesouly the laryngeal

muscles, respiratory muscles and muscles of the mouth

Motor area for controlling hands

More developed on dominant hemisphere R handedness

The process of speech involves

1. Formation of thoughts, selection of wordsWernickes


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2. Motor control of vocalisationBrocas

R hearing a word and repeating it

L reading a word and speaking it

Language Problems

- Auditory receptive aphasia (word deafness) - destruction of auditory cortex

- Visual receptive aphasia (word blindness) - destruction of visual cortex

- Wernickes aphasia - able to hear and understand, can speak with normal grammar, syntax, rate, intonation and stress, but their

language content is incorrect. Unable to formulate the thoughts that are to be communicated. Or, if the lesion is less severe, the

person may be able to formulate the thoughts but unable to put together appropriate sequences of words.

- Global aphasia - damage to wernickes + angular gyrus + inferior temporal gyrus totally demented for language

- Motor/expressive Aphasiadamage to Brocas - can decide what they want to say but cannot force muscles to form words.

- Destruction of 1 motor cortex, basal ganglia, cerebellum all affect speech

9. DESCRIBE THE ANATOMY OF THE CEREBELLUM INCLUDING THE DIFFERENT FUNCTIONAL REGIONS.

3 main fns:

1. Maintenance of posture and balance

2. Maintenance of muscle tone

3. Coordination of voluntary motor activity

3 main parts:

Spinocerebellum

- Receives afferents proprioception

- Maintains muscle tone

- provides the circuitry for coordinating

mainly mvmts of the distal portions of

the limbs, especially the hands and

fingers.

Neocerebellum/Cerebrocerebellum

- Projects to motor cortex

- Helps plan voluntary mvmts

- receives virtually all its input from the

cerebral motor cortex and adjacent

premotor and somatosensory cortices of

the cerebrum.

- transmits its output information in the

upward direction back to the brain,

functioning in a feedback manner with

the cerebral cortical sensorimotorsystem to plan sequential voluntary body

and limb movements

Vestibulocerebellum

- included flocculus and nodulus

- receives input from vestibular Nu

- Maintenance of balance and eye mvmts

via vestibular Nu


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10. DESCRIBE THE ROLE OF THE CEREBELLUM IN CONTROLLING LIMB MOVEMENTS.

3 peduncles

superior cerebellar peduncle (eff>aff) is aka

Brachium ConjunctivumMiddle cerebellar peduncle (Aff) is aka

Brachium PontisInferior cerebellar peduncle (aff=eff) is aka Restiform

Body

Ventral (anterior) spinocerebellar carries

proprioceptive info about the LL golgi tendon organRostral spinocerebellar carries proprioceptive

info (golgi tendon) about the UL

Corticopontinecerebellar- brings motor

information to the cerebellum from thefrontal lobe. Leaves the 1 motor, descends in

the internal capsule along with pyramidal

tract fibres. Its axons synapse with cells in the

pontine nuclei (1st

order neuron). 2nd

order

neurons to the cerebellum via the middle

cerebellar peduncle.

This tract brings the cerebellum a copy of the

information that the corticobulbar and

corticospinal tracts are conveying. The

connection is contralateral

Nucleocerebellar ?

Reticulocerebellar afferent that carries exteroceptiveinformation (visual, olfactory, gustatory, auditory, and

tactile stimuli).

Olivocerebellar?

Arcuateocerebellar- ?

Vestibulocerebellar afferent that carries info from

the vestibular nucleus in the pons and medulla. This

nucleus is fed by the vestibulococclear nerve.

Cerebellothalamic (part of the ascending

pathway)

1. cerebellum dorsal thalamus

2. Thalamus 1 motor

In this way cerebellum performs its comparator fn.

It know the msg sent by the motor cortex (it gets a

copy of the CSp and Corticobulbar via the

corticopontinecerebellar) and it know the actual

action of the muscles (via all the efferents)

It then sends back a msg using this pathway; the

cerebellothalamic, that is able to alter the motor

output.The cerebellorubral pathway does pretty much the

same thing, just stops at the red nucleus on the way

Cerebellorubral(part of the ascending pathway)

1. cerebellum red nucleus in the

midbrain.

2. Red Nu ventrolateral Nu in thalamus.

3. Thalamus 1 motor

See above

Cerebelloreticular (descending pathway) this is

the cerebellar efferent that feeds the reticulospinal

tract

Cuneocerebellar carries proprioceptive info about UL

muscle spindles.

Dorsal (posterior) spinocerebellar carries

proprioceptive info about LL spindle fibres.

Cerebellovesticular (aka cerebellofugal) these carry

impulses to the vestibular Nu. They feed the

vestibulospinal tract.


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Role of Cerebellum in Controlling Limb

Efferent cells of cerebellum do not project to the LMN or brainstem/spinal cord local circuits; they instead modify patterns of UMNs.

1 fn

is to detect motor error and work to reduce this error during the course of the mvmt (feedback) and during subsequent mvmts of this

type (feed-forward)

Inputs

1. Motor planning input: Afferents from the cerebral cortices pontine Nu

cerebrocerebellum

2. Sensory input: Vestibular Nu in medulla project into vesitbulocerebellum +

4xspinocerebellar tract synapse in dorsal Nu of Clarke and project into

spinocerebellum. Ipsilateral via inferior cerebellar peduncle; R cerebellum

concerned R half of body.

Entire cerebellum receives modulation via Inferior olive + locus ceruleus which participate in

the learning and memory fns of the cerebellum.

Projections:

Most efferents project from cortex to deep Nu then out onto target.

1. exception is the vestibulocerebellum to vestibular Nu in medulla (which then

projects to motor cortex).

2. Cerebrocerebellum dentate Nu superior cerebellar peduncle decussate

VNC in thalamus 1 motor cortex + premotor AA

3. Spinocerebellum interposed Nu

4. Vestibulocerebellum fastigial Nu

Cerebellar dx

disrupt the modulation and coordination of ongoing mvmt. Pts have difficultly producing

smooth, well coordinated mvmts cerebellar ataxia

Alcohol anterior degeneration of the cerebellar cortex difficulty in LL mvmts

Vestibulocerebellum lesion difficutly standing upright and maintaining direction of gaze, nystagmus

Spinocerebellar lesions

- difficulty walking b/c of loss of feedback sensory info

- Dysdiadochokinesia = inability to perform rapid alternating mvmts

- Dysmetria = over and under reaching

- Action/intenetion tremors

Cerebrocerebellum

- Impairment in highly skilled sequences of learned mvmt (speech, musical instrument)


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11. DEFINE UPPER AND LOWER MOTOR NEURONS AND DESCRIBE THE CLINICAL FEATURES OF UPPER AND LOWER

MOTOR NEURON LESIONS.

Arranged in 2 tracts

- Lateral group (distal limb, muscles of head) = Rubrospinal +

lateral CSp. Contralateral (mostly)

- Anteriomedial group (trunk) = anterior CSp + tecto, reticulo,

vestibulospinal tracts. Bilateral

Originate from- 1 somatomotor cortex, or unimodal AAs

- 1 somatosensory cortex, unimodal AA

- Brainstem Nu

Cranial and spinal motor nerves are two sets of LMN.

Originate from the anterior horn or the motor Nu of the CNs

2 types

- for extrafusal muscle fibres

- for intrafusal muscle fibres

Inputs

- UMNs- Interneurons

- Sensory input from muscles fibres

UMN lesion LMN lesion

Initially there is spinal shock which causes hypotonia and areflexia

due to sudden in cortical input.

1. Spastic paresis (more common than paralysis)

Spasticity = velocity dependent resistance to passive

movement (clasp knife). cf rigidity which is not velocity

dependent. Due to removal of inhibitory influences on

hyperactive stretch reflexes

2. Hyperreflexia

3. Hypertonia

4. Clonus = rhythmic pattern of contractions due to

alternating stretching and unloading of muscle spindles

5. Loss of dexterity

6. Appearance of primitive reflexes positive Babinski signAtrophy uncommon except when long standing

CLASH Horse

1. Flaccid paralysis (loss of mvmt) more commonly than

paresis (weakness)

2. muscle tone (since tone is modulated by MN and also

influences MN via monosynaptic reflex arc)

3. Fibrillations or fasciculations (aberrant conduction from

damaged neuronal ends and denervation hypersensitivity

due to expression of large number of Ach receptors)

4. Areflexes

5. Muscle wasting (due to denervation and disuse)

Storm Baby

Strength

ToneOther

Reflexes

Muscle mass

Babinski's sign


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12. DESCRIBE THE MAIN CLINICAL FEATURES THAT DIFFERENTIATE OCCLUSION OF ONE OF THE 3 MAIN CEREBRAL

ARTERIES.

ACA: LL>UL paresis and anaesthesia, personality, primitive reflexes (grasp, snout, palmomental), urinary incontinence

MCA M1: UL>LL paresis and anaesthesia, w/b aphasia, alexia, agraphia, acalculia, hemineglect, asterognosia, homonymous hemianopia

PCA: homonymous hemianopia, memory defect, visual agnosia, contralateral hemiparesis, alexia out agraphia

Supplies these areas Thus causes these symptoms

Anterior Cerebral A

- Medial precentral gyrus 1. Contralateral spastic paralysis of lower leg and foot

- Medial postcentral gyrus 2. Contralateral sensory loss of lower leg and foot

- medial frontal 3. Personality changes4. Grasp, snout and palmomental reflexes **

- 5. Urinary incontinence (no clear relationship as to

why)**

- Anterior 4/5 of the corpus callosum

- medial parietal

- medial orbital

- Anterior limb of the internal capsule

- basal ganglia

The severity of an ACA stroke is most dependent on where the occlusion occurs in relation to the

anterior communicating artery

Proximal > distal > bilateral anterior cerebral artery occlusion

> = better prognosis than

A proximal occlusion is normally well tolerated with little to no symptoms.

Grasp, snout and palmomental reflexes

Examples of primitive reflexes exhibited by a child, but normally inhibited by the frontal cortex in an adult.

- Grasp - When an object is placed in the infant's hand and strokes their palm, the fingers will close and they will grasp it.

- Snout - pouting or pursing of the lips that is elicited by light tapping of the closed lips near the midline

- Palmomental - twitch of the chin muscle elicited by stroking a specific part of the palm.

Incontinence in ACA stroke

Damage to the anterior portion of the cingulate gyrus, medial superior frontal gyrus, or the midportion of the superolateral frontal gyrus is

thought to result in this sphincter dysfunction.

Supplies these areas Symptoms Caused

Posterior Cerebral A Occipital 1. Contralateral homonymous hemianopia

Medial temporal 2. Defects in forming new memories

visual association cortex 3. Visual agnosia (inability to recognise familiar objects) and prosopagnosia

(inability to recognise faces)

Cerebral peduncles 4. Contralateral hemiparesis (due to cerebral peduncle infarct - rare)

Splenium of corpus callosum If its in the dominant hemisphere (normally the L)

5. Alexia without agraphia**

Alexia without agraphia

Inability to read but can write. Caused by an infarct to the L PCA (which perfuses the splenium of the corpus callosum and left visual cortex,

among other things). The left visual cortex has been damaged, leaving only the right visual cortex able to process visual information, but it is

unable to send this information to the language areas (Broca's area, Wernicke's area, etc.) in the left brain because of the damage to the

splenium of the corpus callosum. The patient can still write because the pathways connecting the left-sided language areas to the motor areas

are intact.

Supplies these areas Symptoms Caused

Middle Cerebral A Internal capsule

Lateral precentral gyrus Contralateral spastic hemiparesis involving face + arms > legs

Lateral postcentral gyrus Contralateral hemisensory loss involving face + arms > legs

Cortical temporal

- Wernicke's area

- angular gyrus

Fluent ( Wernickes) aphasia**

Alexia (cannot read)

Agraphia (cannot write)

Cortical frontal and parietal

Acalculia (cannot calculate)

Right sided occlusion: left hemineglect**

asterognosis (inability to identify an object by touch out visual

imput)

Contralateral homonymous hemianopia disruption of the optic

radiation in the temporal and parietal white matter.Broca's area Left sided occlusion: nonfluent (Brocas) aphasia**

Basal ganglia See lacunar infarct below.
http://en.wikipedia.org/wiki/Splenium_of_the_corpus_callosumhttp://en.wikipedia.org/wiki/Visual_cortexhttp://en.wikipedia.org/wiki/Broca%27s_areahttp://en.wikipedia.org/wiki/Wernicke%27s_areahttp://en.wikipedia.org/wiki/Spleniumhttp://www.csuchico.edu/~pmccaffrey/syllabi/glossarytz.htm#Wernicke's%20areahttp://www.csuchico.edu/~pmccaffrey/syllabi/glossary.htm#angular%20gyrushttp://www.csuchico.edu/~pmccaffrey/syllabi/glossary.htm#Broca's%20areahttp://www.csuchico.edu/~pmccaffrey/syllabi/glossary.htm#Broca's%20areahttp://www.csuchico.edu/~pmccaffrey/syllabi/glossary.htm#angular%20gyrushttp://www.csuchico.edu/~pmccaffrey/syllabi/glossarytz.htm#Wernicke's%20areahttp://en.wikipedia.org/wiki/Spleniumhttp://en.wikipedia.org/wiki/Wernicke%27s_areahttp://en.wikipedia.org/wiki/Broca%27s_areahttp://en.wikipedia.org/wiki/Visual_cortexhttp://en.wikipedia.org/wiki/Splenium_of_the_corpus_callosum


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Hemineglect

Brain areas in the parietal and frontal lobes are associated with the deployment of attention.

Hemineglect will only happen if the damage is on the non-dominant side (R) because the non-dominant

side of the body is watched by both sides of the brain, whereas the dominant side of the body is only

watched by the non-dominant hemisphere. Said again differently: Right-sided spatial neglect is rare

because there is redundant processing of the right space by both the left and right cerebral hemispheres,

whereas in most left-dominant brains the left space is only processed by the right cerebral hemisphere.

Results in dominant side (L) neglect. Is also accompanied by dominant (L) sided visual neglect.

Wernickes aphasia

Impairment of the comprehension of written and spoken language; can physically speak and even use

words just not in an meaningful way.

Nonfluent Brocas aphasia

Can comprehend text and spoken language but speech is, speech is difficult to initiate, non-fluent, labored, and halting

Lacunar Strokes

Stroke resulting from occlusion of the lenticulostriate arteries (arise from MCA and PCA) that supply the deep structures of the brain.

Depending on which has haemorrhaged will determine the clinical signs seen. These vessels always haemorrhage rather than occlude because

they are weak and very susceptible to pressure

- 37% putamen

- 14% thalamus

- 10% caudate

- 16% pons

- 10% posterior limb of the internal capsule

- less commonly occur in the deep cerebral white matter, the anterior limb of the internal capsule, and the cerebellum.

5 classic syndromes

1. Pure motor stroke of the posterior limb of IC body face = UL = LL + dysphagia + transient sensory symptoms

2. Ataxic hemiparesis of the posterior limb of IC, basis pontis and corona radiata cerebellar and motor symptoms like weakness,

clumsiness,

3. Dysarthria and clumsy hand of the basis pontis dysarthria (speech motor problem1) and clumsiness

4. Pure sensory stroke of the thalamus persistent and transient numbness, tingling, pain, burning, over one side of body

5. Mixed sensorimotor of the thalamus and posterior limb of IC
http://en.wikipedia.org/wiki/Parietal_lobehttp://en.wikipedia.org/wiki/Frontal_lobehttp://en.wikipedia.org/wiki/Speech_communicationhttp://en.wikipedia.org/wiki/Fluencyhttp://en.wikipedia.org/wiki/Putamenhttp://en.wikipedia.org/wiki/Thalamushttp://en.wikipedia.org/wiki/Caudatehttp://en.wikipedia.org/wiki/Ponshttp://en.wikipedia.org/wiki/Internal_capsulehttp://en.wikipedia.org/wiki/Cerebellumhttp://en.wikipedia.org/wiki/Cerebellumhttp://en.wikipedia.org/wiki/Internal_capsulehttp://en.wikipedia.org/wiki/Ponshttp://en.wikipedia.org/wiki/Caudatehttp://en.wikipedia.org/wiki/Thalamushttp://en.wikipedia.org/wiki/Putamenhttp://en.wikipedia.org/wiki/Fluencyhttp://en.wikipedia.org/wiki/Speech_communicationhttp://en.wikipedia.org/wiki/Frontal_lobehttp://en.wikipedia.org/wiki/Parietal_lobe


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13. DESCRIBE AND DIFFERENTIATE BETWEEN THE CLINICAL FEATURES OF UNILATERAL SPINAL CORD, BRAINSTEM,

INTERNAL CAPSULAR AND CORTICAL LESIONS.

Clues Clinical Picture

Unilateral spinal cord

lesion

(aka brown sequard

syndrome)

1. Intact cranial nerves

2. Motor deficits are monoplegic, para, hemi, or quad

3. Sensory sx are contralateral to motor

4. Sensory level may be present

Brown sequard syndrome lateral compression of SC (hemisection)

ipsi/l LMN signs at level of lesion

ipsi/l hemiplegia or monoplegia below lesion & UMN

signs

ipsi/l loss of vibration and proprioception below lesion

contra/l loss of pain and temperature below lesion

common causes tumour, radiation, knife wound

Brainstem lesion Crossed hemiplegia cranial nerve defects 1 side motor sx

other side

Cerebellar findings

Nystagmus

LMN cranial nerve findings

Midbrain = CN 3 ptosis, dilated, down and

out, vertical gaze palsy

Pons = horizontal gaze palsy (INO) +

unilateral facial numbness (CN5) + unilateral

deafness

Medulla-pontine angle - nystagmus

Medulla = bulbar palsy unilateral facial

numbness

Internal capsular lesion Visual field defect

Dystonic postures hyperkinesiasFace and extremity weakness F = UL = LL

Cortical lesion 1. Dysphasia expressive, receptive, global, nominal and

reading (frontal and tempotal lobe)

2. Cortical sensory loss steeognosis, graphesthesia, loss

of 2 point discrimination. (post central gyrus)

3. Face and extremity weakness possible paraesthesia

4. Conjugate gaze palsy 3 gaze centres, 2 in cortex and 1

brainstem. If the eyes deviate together at all the lesion

is cortical, and will deviate to the lesion side

5. seizures


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14. DESCRIBE THE MAJOR SUBTYPES OF STROKE (HAEMORRHAGIC, ISCHAEMIC, THROMBOEMBOLIC) AND THEIR

PATHOLOGICAL CONSEQUENCES.

Stroke =: abrupt onset of focal neurological deficit that is attributed to a focal neurological cause.

Because brain cells lack glycogen, a in blood flow for > a few seconds results in cerebral ischaemia. When blood flow is restored brain tissue

can begin to recover and this is called a transient ischemic attack (=: symptoms resolve in < 24hrs). If cessation of flow lasts > few minutes

then cerebral infarction occurs

Ischaemia

Global cerebral ischaemia

Cause = hypotention, hypoperfusion, low flow states

Result = vulnerable neurons go first and eventually all die persistent vegetative

state/brain dead. Borderzones are the most vulnerable regions at the limits of the

oerlap of blood supply

MORPHO brain swells.

Acute = (12-24hrs) red neurons + PMN infiltrate

subacute = (24-2/52) cell necrosis + M infiltrate, vascular prolif + reactive gliosisRepair = removal of necrotic tissue, loss of CNS structure, gliosis

Focal cerebral ischaemia

Cause =

1. Thrombosis - most common site of atherosclerosis = carotid bifurcation, origin of MCA, either end of basilar artery

a. Hypercoagulopathy s chance of venous (in the brain) and arterial thrombosis (before or in brain)

2. Embolism origin of clot is most commonly cardiac mural thrombi and MI, A Fib and valvular disease are predisposing factors. Next

most common is carotid thrombi. Other = paradoxical emboli

a. Cardioembolic (20%) clot forms on the L atrial, ventricular, valvular wall. RF = A fib, MI, prosthetic valves, RHD, ischaemic

cardiomyopahy

b. Artery to Artery emboli emboli form on atherosclerotic plaque, break off, occlude RF = male, age, smoking, HTN, DM,

hypercholesterolemia, arteristis

c. Arterial dissectionPathophysiology = cells die via

a. necrosis because of energy failure

cells are starved of glucose mitochondria fail to produce ATP

neurons depolarise intracellular [Ca2+

] s membrane and

mitochondrial dysfunction produce free radicals

Fever and hyperglycemia worsen prognosis of dying cells

b. apoptosis

Result =

MORPHO: First 6hrs little observed. By 48hrs tissue is pale, soft,

swollen. Day2-10 brain becomes gelatinous and friable and the

margin btw good and bad tissue is distinct. Day 10- week 3 tissue

liquefies leaving a fluid filled cavity.

MICRO: after first 12hrs you see ischaemic neuronal change (redneurons) + vasogenic and Cytotoxic oedema. Endothelial and glial

cells swell PMN and M infiltrate/activate

Rx:

Mass effect + toxic effect of blood products

Thrombosis, embolism or

vasculitisHypoxia, ischemia, and infarction

Rupture of blood vessel

cerebral blood flow

Focal cerebral ischemia

Global cerebral ischemiahypoxic ischaemic

encephalopahy

haemorrhagic


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Treatment:

- aspirin in 48 hours

- IV tPA in 3 hours

- Intra-arterial (catheter) release of tPA up to 6 hours

- Lowering BP. Only when < 185/110 and thrombolytic

therapy is anticipated OR when there is also myocardial

ischaemia

- Stroke unit for rehab physcial, OT, speech T, education,

Prognosis:

5-10% develop enough brain herniation to cause brain herniation.

Oedema peaks on 2-3 day and is present for 10 days. Cerebellar

infarct and resultant oedema is particularly bad b/c of compression

of brain stem

Rx: water restriction, mannitol, craniotomy

Haemorrhagic

1 haemorrhages in the brain parenchyma or subarachinoid space are typically caused from CV disease., cf edidural and subdural

haemorrhages are 1ly from trauma . These other ones can also be caused by trauma

1. Intercerebral HaemorrhageOriginates in the putamen (50-60%), thalamus, pons, cerebellar. Those originating in the BG are ganglionic haemorrhages cf cerebral

haemorrhages.Acute haemorrhages blood compresses parenchyma cavity eventually occurs with red/brown pigment @ rim central core of clotted

blood surrounded by glial changes, oedema

RF:

a. HTN (50%) - HTN accelerates atherosclerosis in large vessels, hyaline

atherosclerosis in small to medium vessels. May be associated with aneurysm

development

b. Coagulation d/o

c. Open heart surgery, neoplasm, amyloid angiopathy, vasculitis, fusiform

aneurysms, vascular malformations

2. Subarachinoid HaemorrhageMostly from rupture of saccular (berri) aneurysm

Also can be from vascular malformations, extension of a traumatic haematoma, rupture

from HTN, bleeding d/o and tumours.

Berri aneurysms are found in 2% of people. There are other types of aneurysms:

atherosclerotic (fusiform), mycotic, traumatic and dissecting aneurysm. Much less

common.

RF for Berris:

- Genetic, smoking, HTN,

Lacunar Strokes:

a. Pure motor hemiparesis from an infarct in the pos limb of the

IC or basis pontis; the face, arm, and leg are almost always

involved

b. pure sensory stroke from an infarct in the ventrolateral

thalamusc. ataxic hemiparesis from an infarct in the base of the pons

d. dysarthria and a clumsy hand or arm due to infarction in the

base of the pons or in the genu of the IC

e. pure motor hemiparesis with motor (Brocas) aphasia due

to thrombotic occlusion of a lenticulostriate branch supplying

the genu and ant limb of IC and adjacent white matter of the

corona radiata.


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15. IDENTIFY THE MAJOR RISK FACTORS OF CEREBROVASCULAR DISEASE.

Ischaemic Haemorrhage intracerebral or subarachinoid

NONMODIFIABLE MODIFIABLE

Age Arterial HTN

Gender TIAs

Race/ethnicity Prior stroke

Family history Asymptomatic carotid bruit/stenosis

Genetics Cardiac diseaseAortic arch atheromatosis

DM

Dyslipidemia and hypercholesterolemia

Cigarette smoking

Alcohol

Increased fibrinogen

Elevated homocysteine

Low serum folate

Elevated anticardiolipin antibodies

OCP

Obesity

Atrial Fibrillation

NONMODIFIABLE MODIFIABLE

Trauma

Rupture of AV malformation

Ischaemic stroke

HTN

amyloid angiopathyRecreational drug use

Coagulopathy

Tumours

AV malformation

Saccular aneurysm

16. IDENTIFY THE PRINCIPLES OF PATIENT SAFETY IN HEALTH CARE ORGANIZATIONS.

1. We all make errors all the time

2. The health-care system is making errors in patient care, and patients are suffering adverse events, much more than previously

realized.

3. The same error, even a minor one, can have quite different consequences in different circumstances

4. Errors are not intrinsically bad or morally wrong; BUT health-care people expect perfection of themselves, AND our health-care

culture often blames the individual, without looking at the wider picture

17. DISCUSS STRATEGIES TO PROMOTE PATIENT SAFETY IN THE CLINIC.

Clinical Handover

Handovers occur at shift changes, when clinicians take breaks, when pts are transferred, and on admission, referral or discharge

Breakdown of communication is one of the most important contributing factors to adverse events

Solution: The QLD Health Patient Safety and Quality Improvement Service (PSQ) has developed a Clinical Handover Strategy

2010-2013

Coronial Management

Coroners Act 2003 allows for coronial recommendations

3Cs

Correct Patient, Correct Site and Side, Correct Procedure

mandatory standard for all invasive procedures performed in QLD public facilities

Was revised in 2009 to create a four-step protocol:

1. Patient Identification Check

2. Obtaining and Checking Informed Consent

3. Marking and Verfication of Site and Side

4. Team Final CheckClinical Incident Management

Clinical incidents managed according to the Clinical Incident Management Implementation Standard (CIMIS)

Informed Consent

Obtaining informed consent ensures patient safety

Open Disclosure

Is ethically and psychologically important for both patients and staff

Open Disclosure Standard approved by Australian Health Ministers Advisory Council and strongly endorsed by QLD Health

Process: comprises of two components (1) Clinician Open Disclosure and (2) Formal Open Disclosure

Formal Open Disclosure: structured process to ensure communication between patient, senior clinician and the organisation.


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18. IDENTIFY THE PROFESSIONAL OBLIGATION TO DISCLOSE MEDICAL HARM AND ADVERSE EVENTS TO PATIENTS,

OUTLINED IN THE AUSTRALIAN NATIONAL OPEN DISCLOSURE STANDARD (2003).

Legally Healthcare professionals have a duty to inform patients of any error which has made their condition worse (Naylor v Preston Area

Health Authority [1987] 2 All ER 353), especially in situations where a preventable injury will be made worse without further treatment.

Saying sorry to a patient is not legally an admission of guilt and cannot be used to prove liability (in Australia).

The 6 steps of Disclosure:

1. Initial Open Disclosure Team Meeting prior to patient/family meeting.2. Planning between Open Disclosure Consultant and clinician involved or unit director.3. Meeting between patient/family/carer, Open Disclosure Consultantand clinician involved (or unit director).4. Debrief between Open Disclosure Consultantand clinician involved (or unit director) post patient/family/carer meeting.5. Report back to Formal Open Disclosure Team this report summarises any commitments given and how these will be followed up.6. Patient/family/carer support and follow-up of agreed outcomes.

The person making the disclosure should be

a) be known to the patient;

b) be familiar with the facts of the incident and care of the patient;

c) be of sufficient seniority to be credible;

d) have received training in open disclosure;

e) have good interpersonal skills;f) be able to communicate clearly in everyday language;

g) be able and willing to offer reassurance and feedback to the patient and his/her support persons; and

h) be willing to maintain a medium to long-term relationship with the patient where possible.

19. EXPLAIN THE ETHICAL IMPORTANCE OF ACKNOWLEDGING WRONGDOING WHICH HAS CAUSED HARM TO A

PATIENT.

Ethically there are seven reasons to disclose an error:

1. To prevent further harm to the patient

2. To facilitate patient trust

3. It is consistent with the moral obligation of the patient physician relationship

4. It is consistent with social trends towards transparency

5. It manifests for patients as people

6. It enables patients to seek restitution where appropriate

7. It enables efforts to improve patient safety

20. DEMONSTRATE COMPETENCE IN EXPLORING A PATIENT'S EXPERIENCE OF SENSORY DISTURBANCE, MUSCLE

WEAKNESS OR PARALYSIS I NCLUDING:

THE CARDINAL CHARACTERISTICS OF THE SYMPTOM AND ITS TIME COURSE

RELEVANT ASSOCIATED SYMPTOMS

THE PATIENT'S UNDERSTANDING OF, AND CONCERNS ABOUT, WHAT THEY ARE EXPERIENCING

21. DEMONSTRATE COMPETENCE IN THE PHYSICAL EXAMINATION OF A PATIENT FOR THE ASSESSMENT OF RADICULAR

PAIN, SENSORY DISTURBANCE, MUSCLE WEAKNESS, PARALYSIS OR CLUMSINESS IN THE LOWER LIMBS:

DEMONSTRATE APPROPRIATE INFECTION CONTROL MANOEUVRES PRIOR TO AND AFTER EXAMINATION OF A

PATIENT [REVISION]

DESCRIBE THE ANATOMY OF THE MAJOR NERVES OF THE LOWER LIMB AND THE MUSCLE GROUPS OF THE

LOWER LIMB RELEVANT TO CLINICAL EXAMINATION

PREPARE A PATIENT APPROPRIATELY FOR NEUROLOGICAL EXAMINATION IN RELATION TO APPROPRIATE

EXPLANATION, CONFIRMATION OF CONSENT AND PATIENT POSITIONING [REVISION]

OBSERVE THE LOWER LIMBS FOR MUSCLE WASTING, FASCICULATION OR ABNORMAL MOVEMENTS,

COMPARING THE TWO SIDES, THEN DISCUSS THE SIGNIFICANCE OF ANY ABNORMAL FINDINGS

ASSESS THE TONE OF ALL MUSCLE GROUPS IN THE LOWER LIMBS, COMPARING THE TWO SIDES, THEN DISCUSS

THE SIGNIFICANCE OF ANY ABNORMAL FINDINGS

TEST THE POWER OF ALL MUSCLE GROUPS IN THE LOWER LIMBS, COMPARING THE TWO SIDES, THEN DISCUSS

THE SIGNIFICANCE OF ANY ABNORMAL FINDINGS TEST THE KNEE JERKS, ANKLE JERKS AND PLANTAR REFLEXES, COMPARING THE TWO SIDES, THEN DISCUSS THE

SIGNIFICANCE OF ANY ABNORMAL FINDINGS


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TEST THE SENSATION IN THE LOWER LIMBS THROUGH LIGHT TOUCH AND PIN-PRICK, AS WELL AS POSITION

SENSE AT THE HALLUX, USING APPROPRIATE TECHNIQUES AND COMPARING THE TWO SIDES, THEN DISCUSS


DESCRIBE THE DERMATOMES OF THE TRUNK AND LOWER LIMB, AS WELL AS THE SENSORY TERRITORIES OF

THE MAJOR NERVES OF THE LOWER LIMB

RECOGNISE THE COMMON CONDITIONS AFFECTING THE NERVES OF THE LOWER LIMB AND DISCUSS THE

HISTORICAL AND EXAMINATION FEATURES CHARACTERISTIC OF EACH

22. DEMONSTRATE COMPETENCE IN THE PHYSICAL EXAMINATION OF A PATIENT FOR THE ASSESSMENT OF RADICULARPAIN, SENSORY DISTURBANCE, MUSCLE WEAKNESS, PARALYSIS OR CLUMSINESS IN THE UPPER LIMBS:

DEMONSTRATE APPROPRIATE INFECTION CONTROL MANOEUVRES PRIOR TO AND AFTER EXAMINATION OF A

PATIENT [REVISION]

DESCRIBE THE ANATOMY OF THE MAJOR NERVES OF THE UPPER LIMB AND THE MUSCLE GROUPS OF THE

UPPER LIMB RELEVANT TO CLINICAL EXAMINATION

OBSERVE THE UPPER LIMBS FOR MUSCLE WASTING, FASCICULATION OR ABNORMAL MOVEMENTS,

COMPARING THE TWO SIDES, THEN DISCUSS THE SIGNIFICANCE OF ANY ABNORMAL FINDINGS

ASSESS THE TONE OF ALL MUSCLE GROUPS IN THE UPPER LIMBS, COMPARING THE TWO SIDES, THEN DISCUSS


TEST THE POWER OF ALL MUSCLE GROUPS IN THE UPPER LIMBS, COMPARING THE TWO SIDES, THEN DISCUSS


TEST THE BICEPS JERKS, TRICEPS JERKS AND SUPINATOR REFLEXES, COMPARING THE TWO SI DES, THEN

DISCUSS THE SIGNIFICANCE OF ANY ABNORMAL FINDINGS

TEST THE SENSATION IN THE UPPER LIMBS THROUGH LIGHT TOUCH AND PIN-PRICK, USING APPROPRIATE

TECHNIQUES AND COMPARING THE TWO SIDES, THEN DISCUSS THE SIGNIFICANCE OF ANY ABNORMAL

FINDINGS

DESCRIBE THE DERMATOMES OF THE NECK AND UPPER LIMB, AS WELL AS THE SENSORY TERRITORIES OF THE

MAJOR NERVES OF THE UPPER LIMB

RECOGNISE THE COMMON CONDITIONS AFFECTING THE NERVES OF THE UPPER LIMB AND DISCUSS THE

HISTORICAL AND EXAMINATION FEATURES CHARACTERISTIC OF EACH

23. DEMONSTRATE COMPETENCE IN EXPLORING A PATIENT'S EXPERIENCE OF DIZZINESS, FITS, FAINTS OR 'FUNNY

TURNS' INCLUDING: THE CARDINAL CHARACTERISTICS OF THE SYMPTOM AND ITS TIME COURSE; RELEVANT

ASSOCIATED SYMPTOMS, AND THE PATIENT'S UNDERSTANDING OF, AND CONCERNS ABOUT, WHAT THEY ARE

EXPERIENCING. [REVISION]

24. DESCRIBE THE GENERAL PRINCIPLES OF REHABILITATION OF THE OLDER PATIENT WITH STROKE.

Goals of Rehab:

Options for Rehab: Specialist inpatient, outpatient or home-based services

How it works:

Regular team and family meetings are thus mandatory.

Appoint a "key person", one member of the team who liaises with the family; this is also often less intimidating to family members.

Team members: (OPSNNSP)

- Occupational therapists ADLs

- Physiotherapists work muscles- Speech therapists speech, chewing, swallowing

- Nurses bladder and bowel fn

- Neuropsychologist for cognitive deficits like impaired memory and concentration, difficulties in planning and problem solving,

personality , assessment of capacity

- Social workers counselling role with pt and next-of-kin, link professionals in arranging and coordinating community resources.

- Rehabilitation physician team leader and deals with comorbidities (HTN, diabetes), post-stroke depression, pharmacological Rx of

spasticity and pain mgmt.

Documents

Case 1 - Leah French (Stroke)