concepts of neurologic dysfunction chapter 14. alterations in cognitive networks consciousness...
TRANSCRIPT
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