Concepts of Neurologic Dysfunction

Chapter 14

Alterations in Cognitive Networks• Consciousness

– State of awareness of oneself and the environment

– Arousal State of awakeness, loss of thought content

– causes : structural , metabolic or psychological

• Coma is produced by either:– Bilateral hemisphere damage or

suppression– Brain stem lesions or metabolic

derangement

Mosby items and derived items © 2008 by Mosby, Inc., an affiliate of Elsevier Inc.

5 Categories of neurologic function are critical to evaluation process

1. Level of consciousness

2. Pattern of breathing

3. Papillary reaction

4. Oculomotor responses

5. Motor responses

Alterations in Arousal• Clinical manifestations

– Level of consciousness changes– Pattern of breathing

• Posthyperventilation apnea (PHVA) brain regulation to low Paco2

• Cheyne-Stokes respirations (CSR) alteration in tachypnea and apnea

– Vomiting– Pupillary changes- level of brain

dysfunction– Oculomotor responses CN III– Motor responses

Clinical Manifestations

• Ischemia and hypoxia =dilated and fixed• Hypothermia = fixed• Atropine and scopolamine= full dilation and fixed• Sedatives can cause dilated ,unequal or fixed to light

Brain Death (Brain Stem Death)• Body can no longer maintain internal homeostasis• Brain death criteria

– Unresponsive coma (absence of motor and reflex responses)

– No spontaneous respirations (apnea)• Brain death criteria

– No ocular responses– Isoelectric EEG– Persistence for 30 minutes to 1 hour and 6

hours after onset– Confirming test of absent cerebral circulation

Cerebral Death• Cerebral death (irreversible coma) is death of the

cerebral hemispheres exclusive of the brain stem and cerebellum

• No behavioral or environmental responses• The brain can continue to maintain internal

homeostasis

• Survivors of cerebral death– Remain in coma– Emerge into a vegetative state (“wakeful

unconscious state”) – Progress into a minimal conscious state

(MCS)• Locked-in syndrome

Seizures• Sudden, transient alteration of brain function

caused by an abrupt explosive, disorderly discharge of cerebral neurons

• Motor, sensory, autonomic, or psychic signs

• Convulsion– Tonic-clonic (jerky, contract-relax)

movements associated with some seizures

– Aura- hallow effect of vision prior to seizure

– prodromal- early symptoms may occur days before onset

Cognitive Disorders• Selective attention

– Ability to select from available, competing environmental and internal stimuli

– Sensory inattentiveness• Selective attention deficit

• Dysmnesia-– Retrograde amnesia- past memories– Anterograde amnesia-new memories– Executive attention deficits- remembering

instructions

Data Processing Deficits

• Agnosia– Tactile, visual, auditory, etc.

• Aphasia- comprehension or production of language

• Dysphasia- frontal and temporal lobes -written or verbal language

– Expressive dysphasia– Receptive dysphasia– Transcortical dysphasia- repeating and

recite

Acute Confusional States (ACS)

• Acquired mental disorder characterized by deficits in attention and coherence of thoughts and action– Secondary to drug intoxication, metabolic

disorder, or nervous system disease

Dementia

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

Alzheimer Disease (AD)• Familial, early and late onset• Nonhereditary (sporadic, late onset)• Theories

– Mutation for encoding amyloid precursor protein -Senile plaques .Alteration in apolipoprotein E.

– Loss of neurotransmitter stimulation of choline acetyltransferase

• Clinical manifestations– Forgetfulness, emotional upset, disorientation,

confusion, lack of concentration, decline in abstraction, problem solving, and judgment

• Diagnosis is made by ruling out other causes of dementia

Cerebral Hemodynamics

• CBF-cerebral blood flow• CPP- cerebral perfusion pressure• CBV- cerebral blood volume• Cerebral oxygenation• All need to maintained for normal brain

function

Increased Intracranial Pressure (IICP)

• Normal 5 to 15 mm Hg• Caused by an increase in intracranial

content– Tumor growth, edema, excessive CSF,

or hemorrhage• Stage 1• Stage 2• Stage 3• Stage 4

Cerebral Edema

• Increase in the fluid content in brain (intracellular or extracellular) within the brain.

• Brain insult from infections, hemmer rage, tumor, ischemia, brain infarct, or hypoxia.

• Effects of edema can be : distortion of blood vessels, displacement of brain tissue, or herniation of tissue for one brain compartment to another.

Hydrocephalus

• Excess fluid within the cranial vault, subarachnoid space, or both

• Caused by interference in CSF flow– Decreased reabsorption– Increased fluid production– Obstruction within the ventricular system

Alterations in Motor Function

• Muscle tone– Hypotonia- decreased muscle tone– Hypertonia- increase muscle tone– Spasticity-hyperexcitibility of reflexes– Dystonia-sustained involuntary muscle

twisting– Rigidity-tonic reflex , muscles are firm and

tense

Alterations in Movement• Abnormal movements occur in CNS dysfunctions

alter nerve innervations.

• Paresis- ( weakness ) partial paralysis

• Paralysis- loss of motor function

Alterations in Movement Pyramidal motor syndromes• Lower motor neuron syndromes

– Flaccid paresis or flaccid paralysis– Hyporeflexia or areflexia– Fibrillation– Upper motor neuron syndromes

• Hemiparesis or hemiplegia• Diplegia• Paraparesis or paraplegia• Quadriparesis or quadriplegia• Spinal shock

Alterations in Movement

Lower Motor Neuron Syndromes

Amyotrophies- ALS

– Paralytic poliomyelitis– Nuclear palsies– Progressive spinal muscular atrophy– Progressive bulbar palsy– Bulbar palsy

Alterations in Movement

• Hyperkinesia– Excessive movement– Chorea, wandering, tremor at rest, postural

tremor, etc.• Paroxysmal dyskinesias- appear as

involuntary spasms

• Tardive dyskinesia- affect the face ,trunk

Alterations in Movement

• Huntington disease– Also known as “chorea”– Autosomal dominant hereditary-

degenerative disorder onset age 30-40. – Severe degeneration of the basal

ganglia (caudate nucleus) and frontal cerebral atrophy approximately 15 years from onset patient in vegetative state• Depletion of gamma-aminobutyric acid

(GABA)

Alterations in Movement

• Hypokinesia– Decreased movement– Akinesia- loss of voluntary movements due

to loss of dopamine– Bradykinesia– Loss of associated movement

Parkinson Disease

• Severe degeneration of the basal ganglia (corpus striatum) involving the dopaminergic nigrostriatal pathway– Parkinsonian tremor– Parkinsonian rigidity– Parkinsonian bradykinesia– Postural disturbances– Autonomic and neuroendocrine

symptoms– Cognitive-affective symptoms

Parkinson Disease

Disorders of Posture (Stance)

• Dystonia- when muscle groups become unbalanced because of loss of normal posture reflexes,or posturing of limbs– Dystonic - abnormal postures and

movements through muscle contractions– Decorticate posture- hemiplegic posture– Decerebrate posture- head and neck

muscles involved after a severe brain injury– Basal ganglion posture- dysfunctional

equalibrium– Senile posture- increasing flexed posture

Disorders of Posture (Stance)

Disorders of Gait

• Spastic gait- shuffling• Scissors gait- bilateral injury and

spasticity• Cerebellar gait-wide base gait• Basal ganglion and Senile gait- broad

based, small steps and decreased arm swing

Disorders of Expression

• Motor aspects of communication• Hypermimesis-pathological laughter( Rt.

Side hemisphere) or crying Lt. side hemisphere

• Hypomimesis-loss of emotional language

• Dyspraxias and apraxias• – inability to perform purposeful

movements

Disorders of Expression

Extrapyramidal Motor Syndromes

• Basal ganglia motor syndromes• Cerebellar motor syndromes• Both result in movement or postural

disturbances without significant paralysis