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  1. Alterations in Cognitive Networks
    • Full consciousness is an awareness of oneself and the environment with an ability to respond to external stimuli with a wide variety of responses.
    • Consciousness has two components: arousal and content of thought.
    • A decreased level of arousal occurs by diffuse bilateral cortical dysfunction, bilateral subcortical (reticular formation, brain stem) dysfunction, and localized hemispheric dysfunction.
    • An alteration in breathing pattern and level of coma reflect the level of brain dysfunction.
    • Pupillary changes reflect changes in level of brain stem function, drug action, and response to hypoxia and ischemia.
    • Abnormal eye movements, including nystagmus and divergent gaze, reflect alterations in brain stem function.
    • Level of brain function manifests by changes in generalized motor responses or no responses.
    • Loss of cortical inhibition associated with decreased consciousness produce abnormal flexor and extensor movements.
    • Cerebral death or irreversible coma represents permanent brain damage, with an ability to maintain cardiac, respiratory, and other vital functions.
    • Brain death results from irreversible brain damage, with an inability to maintain internal homeostasis.
    • Arousal returns in vegetative states, but content of thought is absent.
    • Seizures represent a sudden, chaotic discharge of cerebral neurons, with transient alterations in brain function. Seizures may be generalized or focal and can result from cerebral lesions, biochemical disorders, trauma, or epilepsy.
    • With a deficit in selective attention, mediated by midbrain, thalamus, and parietal lobe structures, the individual cannot focus on selective stimuli and thus neglects those stimuli.
    • In dysmnesia and amnesia, some past memories are lost and new memories cannot be stored.
    • Frontal areas mediate vigilance, detection, and working memory.
    • With vigilance deficits, the person cannot maintain sustained concentration.
    • With detection deficits, the person is unmotivated and unable to set goals and plan.
    • Some specific disorders or content of thought (cognition) are agnosias, dysphasias, acute confusional states, and dementias.
    • Agnosias are defects of recognition and may be tactile, visual, or auditory. They are caused by dysfunction in the primary sensory area or the interpretive areas of the cerebral cortex.
    • Dysphasia is an impairment of comprehension or production of language. Dysphasia may be expressive or sensory.
    • Aphasia is a loss of language comprehension or production.
    • Wernicke dysphasia is a disturbance in understanding all language, both verbal and reading comprehension.
    • Conductive dysphasias result from disruption of temporal lobe fibers, with a failure to repeat words but an ability to initiate speech, writing, and reading aloud.
    • Anomic dysphasia is an inability to name objects, persons, or qualities.
    • Transcortical dysphasias involve an inability to repeat and recite.
    • Broca aphasia is an expressive dysphasia of speech and writing but with retention of comprehension.
    • Global aphasia involves both anterior and posterior speech areas, with both expressive and receptive aphasia.
    • Acute confusional states are characterized chiefly by a loss of detection and, in the case of delirium, an intense autonomic nervous system hyperactivity.
    • Alzheimer disease is a chronic irreversible dementia that may be related to beta-amyloid metabolism.
    • Pick disease is a rare degenerative disease similar to Alzheimer disease.
  2. Alterations in Cerebral Homeostasis
    • Increased intracranial pressure may result from edema, excess cerebrospinal fluid, hemorrhage, or tumor growth. When intracranial pressure approaches arterial pressure, hypoxia and hypercapnia produce brain damage.
    • Cerebral edema is an increase in the fluid content of the brain resulting from infection, hemorrhage, tumor, ischemia, infarct, or hypoxia.
    • The shifting or herniation of brain tissue from one compartment to another disrupts the blood flow of both compartments and damages brain tissue.
    • Supratentorial herniation involves temporal lobe and hippocampal gyrus shifting from the middle fossa to posterior fossa; transtentorial herniation involves a downward shift of the diencephalon through the tentorial notch; and shifting of the cingulate gyrus can occur under the falx.
    • The most common infratentorial herniation is a shift of the cerebellar tonsils through the foramen magnum.
    • Hydrocephalus comprises a variety of disorders characterized by an excess of fluid within the cranial vault, subarachnoid space, or both. Hydrocephalus occurs because of interference with cerebrospinal fluid flow caused by increased fluid production or obstruction within the ventricular system or by defective reabsorption of the fluid.
  3. Alterations in Motor Function
    • Motor dysfunction may be characterized as alterations of motor tone, movement, and complex motor performance.
    • Hypotonia and hypertonia are the main categories of altered tone.
    • The four types of hypertonia are spasticity, gegenhalten, dystonia, and rigidity.
    • Paresis, paraplegia, hyperkinesias, and hypokinesia are the main categories of altered movement.
    • Two subtypes of paresis/paralysis are described: upper motor neuron paresis/paralysis and lower motor neuron paresis/paralysis.
    • An upper motor neuron syndrome is characterized by paresis/paralysis, hypertonia, and hyperreflexia.
    • Interruption of the pyramidal tract below the pons results in spinal shock.
    • Lower motor neuron syndromes manifest by impaired voluntary and involuntary movements and flaccid paralysis.
    • Partial paralysis occurs with only partial loss of alpha motor neurons, and total paralysis is complete loss of alpha motor neurons. Loss of gamma motor neurons impairs muscle tone and decreases tendon reflexes.
    • Amyotrophy (e.g., poliomyelitis) is a lower motor neuron syndrome involving the anterior horn cells, with loss of muscle tone and strength resulting in segmental paresis and hyporeflexia.
    • Nuclear palsies involve damage to the cranial nerve nuclei.
    • Bulbar palsies involve cranial nerves IX, X, and XII.
    • Included in the category of hyperkinesias are chorea, athetosis, ballism, akathisia, tremor, and myoclonus.
    • Huntington disease (chorea) is a rare hereditary disease involving the basal ganglia and cerebral cortex. It is inherited as an autosomal dominant trait and commonly manifests between 30 and 50 years of age.
    • The major pathologic feature of Huntington disease is severe degeneration of the basal ganglia and the frontal cerebral cortex. The basal ganglia and the substantia nigra exhibit a depletion of gamma-aminobutyric acid (an inhibitory neurotransmitter) secreting neurons. This depletion leads to an excess of dopaminergic activity that causes involuntary, fragmentary movements.
    • Types of hypokinesia include akinesia, bradykinesia, and loss of associated movements.
    • Parkinson disease is a commonly occurring degenerative disorder of the basal ganglia (corpus striatum) involving degeneration of the dopamine-secreting nigrostriatal pathway. The pathogenesis of Parkinson disease is unknown, but researchers suggest genetic, viral, and environmental toxins as possible causes.
    • Degeneration of the dopaminergic nigrostriatal pathway causes dopamine depletion in the basal ganglia and excess of cholinergic activity in the cortex, basal ganglia, and thalamus. Tremor and rigidity are caused by the excess of cholinergic activity. Progressive dementia may be associated with an advanced stage of the disease.
    • Treatment of Parkinson disease is symptomatic involving levodpa (L-dopa), a precursor of dopamine. The disease takes a slowly progressive course for 15 to 20 years.
    • Alterations in complex motor performance include disorders of posture (stance), disorders of gait, and disorders of expression.
    • Disorders of posture include dystonic posture, decerebrate posture, basal ganglion posture, and senile posture.
    • Disorders of gait include upper motor neuron gait, cerebellar gait, basal ganglion gait, and senile gait.
    • Disorders of expression include hypermimesis, hypomimesis, and dyspraxia/apraxia.
    • Dyspraxia is an impairment of the conceptualization or execution of a complex motor act.
    • Extrapyramidal motor syndromes include basal ganglia and cerebellar motor syndromes.
    • Basal ganglia disorders manifest by alterations in muscle tone and posture, including rigidity, involuntary movements, and loss of postural reflexes.
    • Cerebellar motor syndromes result in loss of muscle tone, difficulty with coordination, and disorders of equilibrium and gait.
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14 Notes
2012-05-01 01:08:03

Concepts of Neurologic Dysfunction
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