Altered Consciousness

Altered Consciousnss

Dante P. Bornales, MD, MHPEd Fellow of the Philippine Neurological Association

Consciousness

“awareness of the environment and oneself” “an awake and alert condition” “one is capable of perceiving what’s 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.

Alert

3.

Confused

- transient decline in cognitive functions in the presence of normal arousal; decreased level of attention; impairment of clear thinking

7.

Somnolent

- patient is easily arousable; appropriate verbal and motors responses to sensory stimuli; when left alone patients drifts to sleep state

4.

Obtunded

- alertness is mildly or moderately decreased; when left alone, patient drifts back to sleep state; when aroused, shows slow response to any stimuli

15. Stupor

- moderate amount of spontaneous movements, and can be aroused to respond purposefully to afferent stimuli; can give brief responses to questions or simple commands

6.

- state of extended unconsciousness; unarousable, little or no response to pain or noxious stimuli

Coma

Levels of Depressed Consciousness: M. Victor, A. Ropper: Adams and Victor’s Principles of Neurology, 7th ed.

1.

Alert

3.

Confused

- “clouding of consciousness”; some degree of inattentiveness and disorientation mildly confused moderately confused severely confused

9.

Drowsiness

- inability to sustain a wakeful state without the application of external stimuli; indistinguishable from light sleep

12. Stupor

- 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

5.

- incapable of being aroused by external stimuli semi-coma deep coma

Coma

Levels of Depressed Consciousness: B. Bates: Techniques of Physical Examination, 3rd ed.

2.

Alert

2.

Confused

- mild diminution of consciousness with mental slowness, inattentiveness, dulled perception, incoherent thought process, patient is disoriented

3.

Stupor

- marked reduction in mental and physical activity, marked slowness and reduction in response to commands or stimuli

4.

Coma

- complete loss of consciousness with unresponsiveness to stimuli and voluntary movements

Levels of Depressed Consciousness: W. Demyer: Techniques of the Neurological Examination, 3rd ed.

1.

Alert

3.

Somnolence

- patient can be aroused to a normal level of awareness

6.

Semicoma

- patient can be aroused to some degree, but cannot reach or sustain a normal level of consciousness lethargy stupor

13. Coma

- patient cannot be aroused partial coma deep coma

Glasgow Coma Scale Eye Opening Never To pain To verbal stimuli Spontaneous

1 2 3 4

Best Verbal response No response Incomprehensible sounds Inappropriate words Disoriented Oriented and converses

1 2 3 4 5

Best Motor Response No response Extension/Decerebrate Flexion/Decorticate Flexion withdrawal Localizes Pain Obeys command

1 2 3 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.

Cheyne-Stokes respiration - cerebral hemisphere

2.

CNH - midbrain

3.

Apneustic Breathing - upper pontine level

4.

Ataxic Breathing - medulla oblongata

Clinical Approach to a Comatose Patient

5.

Neurological Assessment

- check pupil responses pin 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 movements do: 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 nerves II and III

Absent pupillary reflexes

III, IV, VI, and VIII

Absent oculocephalic reflex (Doll’s 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

Absent corneal reflexes No facial grimacing to deeply painful facial pain

VIII, III, and VI

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 reflex no 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

“Transient” Loss of consciousness

loss or episodic alteration of consciousness

“Persistent” comatose 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 Consciousness Seizures

•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

Syncope

•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 Consciousness Clinical Features Vertebrobasilar ischemia

Additional brainstem symptoms (eg vertigo, diplopia) Cerebrovascular risk factors Peripheral pulses involvement

Carotid sinus disease

Syncope on turning head or neck or on neck massage Postural hypotension confirmed on tilt table testing

Drop attacks

Elderly females No alteration of consciousness state Rapid recovery Episodic Normal examination and investigation

Hyperventilation

Anxiety or situational (eg. Crowded rooms) Perioral and/or digital tingling sensation, carpopedal spasm, chest pain High respiratory rate, low pCO2, metabolic alkalosis

Sleep disorders • narcolepsy • cataplexy

Inappropriate desire to fall asleep Falls with emotional situations, eg. Laughing Family history

Metabolic (hypoglycemia)

Diabetic on treatment or relative of such a patient Hepatic failure Hypopituitarism, Addison’s disease Insulinemia; glycogen storage disease Excess alcohol

Intracranial Causes of Persistent Alteration of Consciousness Intracranial Causes Epilepsy

Head trauma • extradural or epidural hemorrhage • subdural hemorrhage Cerebrovascular diseases •Subarachnoid hemorrhage

Clinical Features Convulsions 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

• Intracerebral hemorrhage

Presence of focal neurological deficits that are maximal at the onset May have headache, profound alteration of consciousness at the onset

• Hypertensive Encephalopathy

Presence of hypertension, retinopathy, seizures Sudden-onset diffuse (not focal) neurological deficits

Intracranial Causes of Persistent Alteration of Consciousness Intracranial Causes

Infection of the CNS • Meningitis

Clinical Features

Headache prominent early in the course; fever; signs of meningeal irritation

• Encephalitis

Seizures (early encephalitic signs are prominent); fever; presence of profound signs of altered consciousness

• Cerebral abscess

Subacute-onset; headache may be present Focal neurological deficits are present Obvious signs of infections in the contiguous structures

Extracranial Causes of Persistent Alteration of Consciousness Extracranial Causes Circulatory collapse Cardiac causes (arrhythmia, myocardial infarction)

Some Prominent Clinical Features Hypotension, tachycardia, rhythm disturbances; cardiac failure May be preceded by cardiac manifestations (eg. Chest pain; dyspnea)

Septicemic shock

Rigor, pyrexia, vomiting, peripheral vasodilation Obvious source of infection from some other organ system

Hypovolemia (blood loss)

Obvious clinical source of blood loss; tachycardia, pale appearance

Metabolic causes Hypo-or hypernatremia

Muscle twitches, dehydration

Hypo- or hyperkalemia Hypo- or hyperglycemia

Cardiac muscle excitability, ileus, diabetes insipidus

Hemiplegia (reversible), seizures Dehydration, hyperventilation, ketotic breath

Hypo- or hyperthermia

Bradycardia/ initially tachycardia, hypotension, hypoventilation, rigidity, cardiac arrest

Uremia

Sallow skin, pale mucosae, hypertension

Extracranial Causes of Persistent Alteration of Consciousness Extracranial Causes

Some Prominent Clinical Features

Metabolic Causes Hepatic failure Hypoxia Hypercapnia

Endocrine Adrenal Crisis Hypopituitarism

Jaundice, signs of portal hypertension, GI bleeding, sepsis

Following respiratory failure, cardiorespiratory arrest, irreversible brain damage will occur after 4 minutes of anoxia Pink puffer, bounding pulses, papilledema, asterixis

Hypotension, abdominal pain, buccal and flexor pigmentation Pallor, hypogonadism, bitemporal hemianopsia

Extracranial Causes of Persistent Alteration of Consciousness Extracranial Causes Circulatory collapse Cardiac causes (arrhythmia, myocardial infarction)

Some Prominent Clinical Features Hypotension, tachycardia, rhythm disturbances; cardiac failure May be preceded by cardiac manifestations (eg. Chest pain; dyspnea)

Septicemic shock

Rigor, pyrexia, vomiting, peripheral vasodilation Obvious source of infection from some other organ system

Hypovolemia (blood loss)

Obvious clinical source of blood loss; tachycardia, pale appearance

Metabolic causes Hypo-or hypernatremia

Muscle twitches, dehydration

Hypo- or hyperkalemia Hypo- or hyperglycemia

Cardiac muscle excitability, ileus, diabetes insipidus

Hemiplegia (reversible), seizures Dehydration, hyperventilation, ketotic breath

Hypo- or hyperthermia

Bradycardia/ initially tachycardia, hypotension, hypoventilation, rigidity, cardiac arrest

Uremia

Sallow skin, pale mucosae, hypertension

In all comatose patient, attempt to rule out the following conditions: 1. Locked-in syndrome lesion 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 state usually 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. Catatonia silent, no volitional movements no emotional response to external stimuli patient resists an examiner’s attempt to move; patient maintains limbs in fixed position seen in schizophrenic catatonic state

4. Non-convulsive status epilepticus suspect this condition in patients who don’t regain consciousness after a convulsive status epilepticus

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SEIZURE

Seizures •result 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 Prodrome Epilepsy Convulsion

- the seizure event itself - the subjective sensation or any phenomenon that precedes and marks the onset of the epileptic seizure - refers to premonitory changes in mood or behaviour, may precede the attack by some time - recurrent seizure events with definite etiological factor/s - 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 (déjà 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 phase heralded 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 phase violent, 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 neurological disorders • 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 attacks

cardiac 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

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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 frequencies Dementing Diseases

%

Cerebra atrophy, mainly Alzheimer but including Lewy-body, Parkinson, Pick

50

Multi-infarct dementia (Vascular type)

10

Alcoholic dementia

7

Intracranial tumors

5

Normal-pressure hydrocephalus

5

Huntington chorea

2

Chronic drug intoxications

3

Miscellaneous (hepatic failure, pernicious anemia, thyroid

6

diseases, ALS, Creutzfeldt_jacob disease, MS)

Head trauma

2

AIDS dementia

2

Pseudodementias (depression, hypomania, schizophrenia,

8

hysteria, undiagnosed)

M. Victor and A Ropper: Adams and Victor’s 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

Hypothyroidism Hypoparathyroidism

Metabolic

Hepatic Encephalopathy Vit. B12 deficiency

Hydrocephalic

Post-infectious NPH

Tumors

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 ½ of patients with dementia • at least ¼ 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

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