Consciousness

State of awareness of oneself and the surrounding environment

Clinical assessment:

Simple procedure:

– Checking ability to move and react to physical stimuli

– Response in a meaningful way to questions and commands

– Orientation to person, place, time

o Identify name, current location, and current day and time

– Check Level of consciousness (LOC)

Complex procedure:

– Glasgow Coma Scale, based on:

o Eye response

o Verbal response

o Motor response

– Gives cumulative score ranging from 3-15 with 3 being unconscious and 15 normal cognitive function

Alterations in Cognitive Systems – Arousal & Awareness

Arousal: being awake or reactive to stimuli

Awareness: encompasses all cognitive functions

Clinical assessment & impairment

Five categories for assessment:

1. Level of consciousness

o Awake = intact respiration, endocrine, RAS (The reticular activating system) which works with the limbic system (emotions) to coordinate the brain with the environment

2. Pattern of breathing

3. Pupillary changes & eye responses

4. Oculomotor responses

5. Motor responses

o Vomiting, yawning, hiccups

Acute Confusional States (ACS) – Delirium

Transient disorder of awareness that result from cerebral dysfunction

Causes:

Secondary to drug intoxication, metabolic disorder, or nervous system disease

Common in post-op patients

Increased in elderly population

Types

Hyperkinetic – They pull IV lines, get out of their hospital bed

Hypokinetic – Flaccid, no response to anything

Brain Death

Brain can no longer maintain internal homeostasis

– Absence of functioning in brain including the brainstem and cerebellum

– Condition observed for an extended period of time

Brain death criteria:

Established etiology capable of causing neurological death in the absence of reversible conditions capable of mimicking neurological death

Unresponsive coma with bilateral absence of motor responses, excluding spinal reflexes

No brainstem function

No spontaneous respiration (apnea)

Absence confounding factors

– Occurs because of known structural defect or metabolic disease

Cerebral Death

Cerebral death (irreversible coma) is death of the cerebral hemispheres exclusive of the brainstem and cerebellum

No behavioural or environmental responses

The brain can continue to maintain internal homeostasis

Survivors of cerebral death:

– Remain in coma

– Emerge into a persistent vegetative state

– Progress into a minimally conscious state (MCS)

– *The patient will never regain behavioural responses to stimuli*

Seizures

Sudden (definitive feature), transient, excessive electric activity within the brain (neuron firing)

Can be motor, sensory, autonomic, or psychic in nature

Can be partial (focal) or generalized

Etiology

Etiologic factors are wide and diverse in range

Epilepsy:

– A specific chronic CNS disease of abnormal brain activities characterized by ≥ 2 unprovoked seizures to make a diagnosis

– Seizure activity with no underlying, diagnosable cause

– Affects both males and females of all races, ethnic backgrounds and ages.

– Symptoms can vary widely from simply stare blankly for a few seconds during a seizure, repeated twitches of arms or legs or severe lasting ones

CNS lesions, including:

– Meningitis

– Multiple sclerosis (MS)

– Tetanus

– Trauma

Biochemical disorders including:

– Elevated bilirubin in children

– Fever

– Encephalitis

– Electrolyte imbalance

– Hypoglycemia

– Lead poisoning

Manifestations

Loss of consciousness

Sudden loss of autonomic control

– Incontinence is common and can be embarrassing for the person when they recover

Convulsions: Jerky (rapid and repeated) contract-relax body movements

– Also called tonic-clonic seizures

Aura: Perceptions experienced a few seconds-hours before seizure (or migraine) begins

– Examples: strange light, unpleasant smell or confusing thoughts

A seizure is NOT a disease, it is a manifestation within a larger disorder

Data Processing Deficits

The brain is responsible for receiving, processing, and interpreting data from sensors throughout the body

– Brodmann’s cytoarchitectural map identifies, generally, specialized areas of the

brain used for receiving and processing this data

Agnosia: Inability to process sensory information and recognize form and nature of objects

– Poor recognition

– May be tactile, visual, auditory, etc., or a combination depending on the areas of the brain impacted

Dysphasia: Impairment of production or comprehension of language

– Reduced ability to speak, read, or write

– Classified both anatomically and functionally including:

o Expressive dysphasia

o Receptive dysphasia

o Transcortical dysphasia

• Person is able to repeat (echolalia) and recite with fluent speech, however comprehension is impaired, and speech makes no sense

• They are unable to read or write in their own language

– Aphasia: Severe form of dysphasia whereby the person is unable to communicate

o Example: A person can see the glass in their hands, they know what it is, but they cannot verbally tell you they are holding a glass

Dementia

Progressive failure of cerebral functions that is not caused by an impaired level of consciousness

Often includes decreased functioning and losses in:

– Orientation

– Memory

– Language

– Judgment

– Decision making

As intellectual function declines, the person will exhibit behaviour changes becoming more repetitive, obsessive, and decline in social functioning

Causes:

Alzheimer disease

– Most famous (see below)

Vascular dementia

Dementia with Lewy bodies (DLB)

Mechanisms:

Neuron degeneration

Brain tissue compression

Atherosclerosis

Brain trauma

CNS infections

– Such as HIV and slow-growing viruses associated with Creutzfeldt-Jakob disease

Genetic predisposition associated with neurodegenerative diseases

Alzheimer Disease (AD)

Structural changes in the brain leading to dramatic decline in intellectual functions.

Etiology

Unknown, however there is a genetic link to Chromosome 21 in those with early onset AD and chromosome 19 in those with late onset

Pathophysiology

Premature neuron death and cellular changes, characterized by:

– Amyloid plaques accumulates in extracellular spaces

– Neurofibrillary tangles (twisted bundles of filaments) intracellularly

– Intracellular vacuoles leading cellular swelling and death with shrinkage of brain matter

acetyltransferase

Clinical manifestations:

Forgetfulness

Emotional upset

Disorientation

Confusion

Lack of concentration

Decline in abstraction, problem solving, and judgment

Rule-out diagnosis

– Diagnosis is made by ruling out other causes of dementia

– The only definitive diagnosis can be made on autopsy

Cerebral Hemodynamics

Basics

Cerebral blood flow (CBF): Amount of blood flow to the brain

– Maintained at a rate required to meet metabolic needs

– Constitutes 15% of cardiac output

– Calculated by the formula CBF = CPP/CVR

Cerebral perfusion pressure (CPP): Pressure required to perfuse cells of brain

– Calculated by the formula CPP =MAP-ICP

Intracranial pressure (ICP)

– Normally 5 to 15 mmHg

Increased Intracranial Pressure (IICP)

Caused by increase in intracranial content

– For example, tumor, edema, excessive CSF, or hemorrhage

Stages:

Stage 1

– Minimal increase in ICP

– Usually compensated

Stage 2

– Systemic arteriolar vasoconstriction to increase MAP and CPP and maintain neuronal oxygenation

Stage 3

– Sustained increased ICP approaching MAP

Cerebral Edema

Increase in the fluid (intracellular or extracellular) within the brain

Causes:

Brain trauma

Non traumatic causes

– Ischemic stroke

– Cancer

– Inflammation (meningitis/encephalitis)

Pathophysiology and Types:

Vasogenic:

– Disruption of blood brain barrier (BBB)

– Intravascular proteins and fluid escape to brain parenchyma

Cytotoxic:

– BBB remains intact, toxins impair cellular metabolism

Interstitial:

– Disruption of Blood-CSF barrier

– CSF flows to interstitial space

Hydrocephalus

Abnormal accumulation of CSF in the ventricles, subarachnoid space within the brain

Pathophysiology and features:

Interference in CSF flow

Increased intracranial pressure

Head enlargement

Impairment of cognitive functions

– Related to increased compression on neuronal axons and decreased oxygen perfusion and ICP increases

Treatment

Shunt inserted to drain fluid

Alterations in Movement – Terminology

Upper motor neuron syndromes:

Hemiparesis or hemiplegia

Diplegia

Paraparesis or paraplegia

Quadriparesis or quadriplegia

Lower motor neuron syndromes:

Flaccid paresis or flaccid paralysis

Hypertonia and hypotonia

Hyperkinesia

– Excessive, purposeless movement

Paroxysmal dyskinesias

– Abnormal, involuntary movements that occur as spasms

Tardive dyskinesia

– Involuntary movement of face, lip, tongue, trunk, and extremities

– Usually a side effect of antipsychotic medication

Hypokinesia, Akinesia, Bradykinesia

– Slowed or absent movement

Huntington Disease

Autosomal dominant degenerative disorder

Pathophysiology:

CAG repeats in Huntington gene located on chromosome 4

There is depletion of gamma-aminobutyric acid (GABA) (an inhibitory transmitter)

– Leads to increase in involuntary movement

Severe degeneration of the basal ganglia (caudate nucleus) and cerebral cortex

Clinical manifestations:

Chorea (characteristic manifestation)

– Non-repetitive muscular contractions, usually in the extremities of the face

– Random, irregular pattern of rapid, involuntary muscular contractions

– Decreases with sleep and rest

– Increases with emotional stress and attempted voluntary movement

– Related to changes occurring at the level of the basal ganglia

General restlessness, lack of coordination, involuntary eye movements

Subtle changes in personality, emotion, cognition abilities

Parkinson Disease

A common chronic and progressive neurodegenerative disorder

Pathophysiology:

Severe degeneration of the basal ganglia

Diminished dopamine released by substantia nigra

Thalamus and globus palladium become overactive resulting in motor impairments

Clinical Manifestations:

Parkinsonian tremors, rigidity, bradykinesia

Postural disturbances

Autonomic and neuroendocrine symptoms

Cognitive-affective symptoms

Disorders of Posture, Gait & Expression – Terminology

Disorders of Posture (Stance):

Dystonia:

– Maintenance of abnormal postures through muscular contractions

– Dystonic and associated movements

o Dystonic movements last seconds while dystonic postures are held for longer periods

Decorticate:

– Flexion inwards towards ‘core’ of body

Decerebrate:

– Extension outwards from body

Basal ganglion

Senile:

– Increased flexed posture similar to basal ganglion

Disorders of Gait

Spastic gait:

– Shuffling gait with one leg extended and the other held stiff, which can often lead to it being dragged

– Associated with unilateral injury

Scissors gait:

– Legs adducted so they touch and then swing around each other

– Associated with bilateral injury and spasticity

Cerebellar gait:

– Wide base with feet often turned inward or

outward for stability

Basal ganglion gait:

– Stooped, hyperflexed posture with narrow base and short-stepped gait with decreased arm swing

Senile gait:

– Similar to the basal ganglion gait

Disorders of Expression:

Hypermimesis:

– Pathologic laughter or crying

Hypomimesis:

– Loss of emotion in language (arhapsody)

– Also, receptive arhapsody where the person is unable to understand emotional speech and facial expressions

Dyspraxias and apraxias:

– Difficulty planning and executing coordinated motor movements

o Examples of tasks include speaking, writing, using tools/utensils, playing sports, following instructions, and the ability to focus

– May be developmental or associated with vascular disorders (common in stroke), trauma, infection, tumors, degenerative disorders

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