Altered Consciousnss
Consciousness
awareness of the environment and oneself an awake and alert
condition one is capable of perceiving whats happening in the
surroundings ability to respond in an appropriate manner to certain
stimuli
components of consciousness: 1. arousal and wakefulness -
functions of the ARAS and its projections 2. awareness or the
content of consciousness - function of the cerebral cortex
representing cognitive mental functions
Structures comprising the Consciousness System:1. Reticular
formation 2. Neurochemically-defined nuclear groups of the
brainstem 3. Thalamus and the thalamic nuclei 4. Thalamocortical
pathway (tract) 5. Basal forebrain 6. Cerebral cortical areas
Levels of Depressed Consciousness:E. Benarroch, B. Westmoreland,
et al: Medical Neurosciences, 3rd ed.
1. 3.
Alert Confused - transient decline in cognitive functions in the
presence of normal arousal; decreased level of attention;
impairment of clear thinking - patient is easily arousable;
appropriate verbal and motors responses to sensory stimuli; when
left alone patients drifts to sleep state - alertness is mildly or
moderately decreased; when left alone, patient drifts back to sleep
state; when aroused, shows slow response to any stimuli - moderate
amount of spontaneous movements, and can be aroused to respond
purposefully to afferent stimuli; can give brief responses to
questions or simple commands - state of extended unconsciousness;
unarousable, little or no response to pain or noxious stimuli
7.
Somnolent
4.
Obtunded
15. Stupor
6.
Coma
Levels of Depressed Consciousness:M. Victor, A. Ropper: Adams
and Victors Principles of Neurology, 7th ed.
1. 3.
Alert Confused - clouding of consciousness; some degree of
inattentiveness and disorientation mildly confused moderately
confused severely confused - inability to sustain a wakeful state
without the application of external stimuli; indistinguishable from
light sleep - can be roused only by vigorous and repeated stimuli,
at which time, patient opens his eyes, looks at the examiner, and
does not appear to be unconscious - incapable of being aroused by
external stimuli semi-coma deep coma
9.
Drowsiness
12. Stupor
5.
Coma
Levels of Depressed Consciousness:B. Bates: Techniques of
Physical Examination, 3rd ed.
2. 2.
Alert Confused - mild diminution of consciousness with mental
slowness, inattentiveness, dulled perception, incoherent thought
process, patient is disoriented - marked reduction in mental and
physical activity, marked slowness and reduction in response to
commands or stimuli - complete loss of consciousness with
unresponsiveness to stimuli and voluntary movements
3. 4.
Stupor Coma
Levels of Depressed Consciousness:W. Demyer: Techniques of the
Neurological Examination, 3rd ed.
1. 3. 6.
Alert Somnolence Semicoma - patient can be aroused to a normal
level of awareness - patient can be aroused to some degree, but
cannot reach or sustain a normal level of consciousness lethargy
stupor - patient cannot be aroused partial coma deep coma
13. Coma
Glasgow Coma ScaleEye Opening Never To pain To verbal stimuli
Spontaneous Best Verbal response No response Incomprehensible
sounds Inappropriate words 3 Disoriented Oriented and converses
Best Motor Response No response Extension/Decerebrate
Flexion/Decorticate 3 Flexion withdrawal Localizes Pain Obeys
command
1 2 3 4 1 2 4 5 1 2 4 5 6
Clinical Approach to a Comatose Patient
1.
Airway-Breathing-Circulation Endotracheal intubation /
oropharyngeal tube Intravenous fluids Do: a rapid neurological
assessment while addressing the vital functions Do: initial ocular
survey of the organ-systems of the body while addressing A-B-C
2. General Physical Examination signs of head injury look for
meningeal signs of irritation
Clinical Approach to a Comatose Patient
1.
Neurological Assessment Always Inspect! Note for limb movement
asymmetry position of head and eyes; facial grimacing to a given
stimulus state of responsiveness / level of consciousness / GCS
involuntary movements of limbs abnormal posturing
Decorticate Posturing Vs Decebrate posturing
Clinical Approach to a Comatose Patient
4.
Neurological Assessment Inspect! abnormal breathing patterns
Sites of the lesions: 1. 2. 3. 4. Cheyne-Stokes respiration -
cerebral hemisphere CNH - midbrain Apneustic Breathing - upper
pontine level Ataxic Breathing - medulla oblongata
Clinical Approach to a Comatose Patient
5.
Neurological Assessment
- check pupil responsespin point - pontine hemorrhage; opiate
poisoning bilaterally fixed mid position - midbrain lesion
unilateral or bilateral fixed and dilated - supratentorial mass
with uncal herniation enlarged, slowly reactive pupils - metabolic
causes
- examine ocular movementsdo: oculocephalic reflex
oculovestibular reflex
- examine the fundi (fundoscopic examination)look: papilledema;
subhyaloid hemorrhage
Useful guide in the examination of the brainstem/cranial nerve
functions in a comatose patient
Cranial nervesII and III III, IV, VI, and VIII Absent pupillary
reflexes Absent oculocephalic reflex (Dolls eye maneuver)the eye
moves passively in the direction of the horizontal or vertical eye
movements, rather than maintaining their positions of gaze while
the head is being moved by the examiner
V and VII VIII, III, and VI
Absent corneal reflexes No facial grimacing to deeply painful
facial pain Absent water caloric reflexes (oculovestibular
responses)an intact reflex consists of transient tonic deviation of
the eyes towards the stimulated side when stimulated with cold
water
IX and X
Absent gag reflexno cough or gag in response to pharyngeal or
tracheal stimulation and suctioning
Absence of any respiratory effort, even after fully oxygenating
the patient and then allowing the pCO2 to rise to 50-60 mmHg (apnea
test)
Altered Consciousness
TransientLoss of consciousness
loss or episodic alteration of consciousness
Persistentcomatose state Transient loss of consciousness
seizures syncope cerebral ischemia / vertebrobasilar ischemia
carotid sinus disease drop attacks sleep disorders metabolic
(hypoglycemia)
Differential Diagnosis of Transient Loss of
ConsciousnessSeizures Syncope
can occur in any position and time of the day Preceding aura may
be present Sudden-onset Urinary or fecal incontinence may be
present Tongue bitting Post-ictal confusion, drowsiness, and
headache
upright position usually prodrome light headed, nausea, ringing
in the ears, dimming of vision, pallor, sweating hypotension and
thready pulses relatively rapid recovery
Situational syncope: Emotion or pain Micturition Coughing
Postural
Cardiac causes of syncope:
Left or right ventricular outflow obstruction Arrhythmias pump
failure
Differential Diagnosis of Transient Loss of
ConsciousnessClinical Features Vertebrobasilar ischemiaAdditional
brainstem symptoms (eg vertigo, diplopia) Cerebrovascular risk
factors Peripheral pulses involvement Syncope on turning head or
neck or on neck massage Postural hypotension confirmed on tilt
table testing Elderly females No alteration of consciousness state
Rapid recovery Episodic Normal examination and investigation
Anxiety or situational (eg. Crowded rooms) Perioral and/or digital
tingling sensation, carpopedal spasm, chest pain High respiratory
rate, low pCO2, metabolic alkalosis Inappropriate desire to fall
asleep Falls with emotional situations, eg. Laughing Family history
Diabetic on treatment or relative of such a patient Hepatic failure
Hypopituitarism, Addisons disease Insulinemia; glycogen storage
disease Excess alcohol
Carotid sinus disease Drop attacks
Hyperventilation
Sleep disorders narcolepsy cataplexy Metabolic
(hypoglycemia)
Intracranial Causes of Persistent Alteration of
ConsciousnessIntracranial Causes Epilepsy Clinical
FeaturesConvulsions that are clinically unequivocal May have
incontinece Tongue biting and other injuries may be present
Evidence of head injury or presence of basal skull fracture Remote
history of head injury (several weeks or even months) Elderly
patients and alcoholics are at particular risk, eg prone to
accidental falls History of sudden severe/explosive headache
Associated with an initial loss of consciousness (collapse)
Presence of fever (central in origin) Neck rigidity; presence of
meningeal irritation Focal neurological deficits particularly if
with intracerebral extension or complications Presence of focal
neurological deficits that are maximal at the onset May have
headache, profound alteration of consciousness at the onset
Presence of hypertension, retinopathy, seizures Sudden-onset
diffuse (not focal) neurological deficits
Head trauma extradural or epidural hemorrhage subdural
hemorrhage Cerebrovascular diseases Subarachnoid hemorrhage
Intracerebral hemorrhage Hypertensive Encephalopathy
Intracranial Causes of Persistent Alteration of
ConsciousnessIntracranial Causes Clinical Features
Infection of the CNS Meningitis Encephalitis
Headache prominent early in the course; fever; signs of
meningeal irritation Seizures (early encephalitic signs are
prominent); fever; presence of profound signs of altered
consciousness Subacute-onset; headache may be present Focal
neurological deficits are present Obvious signs of infections in
the contiguous structures
Cerebral abscess
Extracranial Causes of Persistent Alteration of
ConsciousnessExtracranial Causes Circulatory collapse Cardiac
causes (arrhythmia, myocardial infarction) Septicemic shock
Hypovolemia (blood loss) Metabolic causes Hypo-or hypernatremia
Hypo- or hyperkalemia Hypo- or hyperglycemia Some Prominent
Clinical FeaturesHypotension, tachycardia, rhythm disturbances;
cardiac failure May be preceded by cardiac manifestations (eg.
Chest pain; dyspnea) Rigor, pyrexia, vomiting, peripheral
vasodilation Obvious source of infection from some other organ
system Obvious clinical source of blood loss; tachycardia, pale
appearance Muscle twitches, dehydration Cardiac muscle
excitability, ileus, diabetes insipidus
Hemiplegia (reversible), seizures Dehydration, hyperventilation,
ketotic breath Bradycardia/ initially tachycardia, hypotension,
hypoventilation, rigidity, cardiac arrest Sallow skin, pale
mucosae, hypertension
Hypo- or hyperthermia Uremia
Extracranial Causes of Persistent Alteration of
ConsciousnessExtracranial Causes Metabolic Causes Hepatic failure
Hypoxia HypercapniaJaundice, signs of portal hypertension, GI
bleeding, sepsis
Some Prominent Clinical Features
Following respiratory failure, cardiorespiratory arrest,
irreversible brain damage will occur after 4 minutes of anoxia Pink
puffer, bounding pulses, papilledema, asterixis
Endocrine Adrenal Crisis Hypopituitarism
Hypotension, abdominal pain, buccal and flexor pigmentation
Pallor, hypogonadism, bitemporal hemianopsia
Extracranial Causes of Persistent Alteration of
ConsciousnessExtracranial Causes Circulatory collapse Cardiac
causes (arrhythmia, myocardial infarction) Septicemic shock
Hypovolemia (blood loss) Metabolic causes Hypo-or hypernatremia
Hypo- or hyperkalemia Hypo- or hyperglycemia Some Prominent
Clinical FeaturesHypotension, tachycardia, rhythm disturbances;
cardiac failure May be preceded by cardiac manifestations (eg.
Chest pain; dyspnea) Rigor, pyrexia, vomiting, peripheral
vasodilation Obvious source of infection from some other organ
system Obvious clinical source of blood loss; tachycardia, pale
appearance Muscle twitches, dehydration Cardiac muscle
excitability, ileus, diabetes insipidus
Hemiplegia (reversible), seizures Dehydration, hyperventilation,
ketotic breath Bradycardia/ initially tachycardia, hypotension,
hypoventilation, rigidity, cardiac arrest Sallow skin, pale
mucosae, hypertension
Hypo- or hyperthermia Uremia
In all comatose patient, attempt to rule out the following
conditions: 1. Locked-in syndromelesion in the ventral pons
affects: corticobulbar and corticospinal tracts patient is awake
but unable to respond patient communicates via vertical eye
movements and blinking
2. Persistent vegetative stateusually secondary to severe
cerebral injury patient recovers partially from a comatose state no
purposeful movements and no demonstrable cognitive functions
In all comatose patient, attempt to rule out the following
conditions: 3. Catatoniasilent, no volitional movements no
emotional response to external stimuli patient resists an examiners
attempt to move; patient maintains limbs in fixed position seen in
schizophrenic catatonic state
4. Non-convulsive status epilepticussuspect this condition in
patients who dont regain consciousness after a convulsive status
epilepticus
End of segment
SEIZURE
Seizuresresult from abnormal, sudden, excessive and asynchronous
electrical discharges from the cortical neurons the discharges are
self-terminating and have a tendency to recur
Ictus Aura
- the seizure event itself - the subjective sensation or any
phenomenon that precedes and marks the onset of the epileptic
seizure Prodrome - refers to premonitory changes in mood or
behaviour, may precede the attack by some time Epilepsy - recurrent
seizure events with defin ite etiological factor/s Convulsion -
seizure events with motor manifestations
Seizures
Seizures
Partial seizures- deviation of the head and eyes to one side
(aversive seizure) points to an irritative focus in the opposite
prefrontal region
- in simple partial seizures, consciousness is often preserved
(see video) - Jacksonian seizure starts as a clonic movement in one
portion of the body, usually the thumb, corner of the mouth, or
great toe, and spreads to adjacent muscular groups over a few
seconds or minutes - the seizure event may persist on one part of
the body or may become generalized
Complex partial seizures -differs from generalized motor
seizures by:1. frequent occurrence of an aura that arises from
discharges in the autonomic, visceral, olfactory portions of the
temporal lobe and limbic system 2. loss of awareness or contact
with the environment, often associated with behavioral or complex
motor movements for which the patient is amnesic after the
attacks
Complex partial seizures
Complex partial seizures
- subjective experiences of the aura:hallucinations (olfactory,
gustatory, visual, auditory) illusions (space distortions,
shrinkage, or angulations) aberrations in cognition (dj vu, sense
of familiarity) affective changes (anxiety, fear, rage)
- the seizure may terminate with only the subjective component
or may progress to the motor phase evident by repetitive motor acts
(chewing, lip smacking, undressing, incoherence)
Tonic-clonic (grand mal) seizures- abrupt-onset, w/o warning;
usually begin with opening of the eyes and mouth, flexion and
abduction of the arms, and extension of the legs tonic
phaseheralded by contraction of the respiratory muscles resulting
in vocalization; followed by closure of the jaw, respiratory arrest
with cyanosis, and sphincter incontinence persists for about 15-30
sec. followed immediately by the clonic phase
clonic phaseviolent, rhythmic muscular contractions affecting
the whole body and respiratory muscles eye movements, facial
grimacing, persistent apnea lasts for about 1-2 min.
Tonic-clonic (grand mal) seizures
Absence seizures- brief; loss of contact with the environment
accompanied by minimal motor manifestations - abrupt in onset and
described as a stare or cessation of an ongoing behavior - may be
accompanied by fluttering of the eyelids or by few facial twitches
- full recovery is evident after 5-10 sec.
Absence seizures
Etiology epilepsy is a symptom and sign of numerous
neurologicaldisorders over 50% of patients have no apparent cause
can be found despite full and extensive investigation etiology will
greatly vary depending on: - the age of the patient - surrounding
circumstances in the history
Causes of seizures
The following are the most common differential diagnoses In a
patient presenting with seizures: syncopal attackscardiac
arrhythmias, carotid sinus hypersensitivity, vasovagal attacks,
postural hypotension present are: prodromal pallor, nausea,
vomiting, sweating, palpitations
pseudoseizures
hysterical, attention-seeking, feigned seizures are common
especially in patients with known seizures vital signs, pupils, pO2
and serum pH remain unchanged, plantar responses are normal, the
EEG will reveal normal findings and no postictal cortical activity
slowing
transient ischemic attacks / cerebrovascular diseases metabolic
causes, eg. hypoglycemia
End of segment
Dementia Dementia (WHO ICD-10) a disorder characterized by both
memory and thinking deterioration sufficient to impair personal
activities of daily living; the memory impairment affects the
registration, storage and retrieval of new information
not a disease entity, rather a symptomatology with varied
etiology and clinical presentation impaired consciousness implies
delirium rather than dementia the most common causes are Alzheimer
and Vascular dementia, both are seen in advanced age groups
Common types of dementing diseases and their approximate
frequenciesDementing Diseases Cerebra atrophy, mainly Alzheimer but
including Lewybody, Parkinson, Pick Multi-infarct dementia
(Vascular type) Alcoholic dementia Intracranial tumors
Normal-pressure hydrocephalus Huntington chorea Chronic drug
intoxications Miscellaneous (hepatic failure, pernicious anemia,
thyroid diseases,ALS, Creutzfeldt_jacob disease, MS)
% 50 10 7 5 5 2 3 6 2 2 8
Head trauma AIDS dementia Pseudodementias (depression,
hypomania, schizophrenia,hysteria, undiagnosed)
M. Victor and A Ropper: Adams and Victors principles of
Neurology 7th ed.
Dementia
General clinical features: The earliest feature of dementia,
from most causes, is loss of memory for recent events. Subsequent
symptoms include abnormal behavior, loss of intellect, mood
changes, and difficulty coping with ordinary routines. Rate of
progression: Alzheimer disease Vascular dementia Encephalitis -
slowly progressive over years - progressive but often fluctuating
or stepwise with each stroke - over days to weeks
Some reversible forms of dementia: Endocrinologic Metabolic
Hydrocephalic Tumors Hypothyroidism Hypoparathyroidism Hepatic
Encephalopathy Vit. B12 deficiency Post-infectious NPH
Meningiomas
Pseudodementia Major Depression
Things to emphasize in the History and Examination of a demented
patient:It is essential to get a history from a relative or friend,
as well as from the patient in order to gauge the following rate of
intellectual decline activities of daily living and social
interaction nutritional status drug history general health and
relevant disorders, eg. Stroke, head injury family history of
dementia
Neurologic evaluation should focus more on the following
presence of focal neurologic deficits involuntary movements
pseudobulbar signs presence of primitive reflexes, eg. Pout, grasp
reflexes gait disorder
Things to emphasize in the History and Examination of a demented
patient:Neurologic evaluation should focus more on the following
presence of focal neurologic deficits involuntary movements
pseudobulbar signs presence of primitive reflexes, eg. Pout, grasp
reflexes gait disorder
In all patients suspected with dementia, it is essential to
utilize the Mini-mental State Scale
Probable dementia = 24-27 score
Primary degenerative dementia: 1. Alzheimer disease 2. Pick
disease 3. Lewy-body dementia
Alzheimer disease accounts for more than of patients with
dementia at least of the population over 85 years have Alzheimer
Clinical symptomatology: short term memory loss > long term
memory personality changes depression anxiety other psychological
features
Alzheimer disease Clinical signs:Early stages - will reveal very
little clues - slight confusion on dates and location of the
interview - speech can be a little hesitant - no focal neurological
deficits Later stages - as the disease progresses, problems in
language, praxis and gnosis become increasingly apparent - personal
care deteriorates - primitive reflexes emerge - eventually, the
patient becomes mute, bed-bound and incontinent - condition
generally lasts 7-15 years
Parting words on Alzheimer disease typically, a patient with
Alzheimer disease does not initiate the consultation there are
seldom any focal neurological signs at the time of the first
assessment formal psychometry is usually essential to confirm the
diagnosis, rather than relying only on the screening test such as
the MMSE scale the main role of brain imaging in the assessment of
Alzheimer Is to exclude other treatable or revesible dementias
End of segment
