Download presentation
Presentation is loading. Please wait.
Published byMeagan Lambert Modified over 8 years ago
1
Concepts of Neurologic Dysfunction Chapter 14
2
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
3
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 Mosby items and derived items © 2008 by Mosby, Inc., an affiliate of Elsevier Inc.
4
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
5
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
6
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
7
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
8
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
9
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
10
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
11
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
12
Dementia Progressive failure of cerebral functions that is not caused by an impaired level of consciousness
13
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
14
Cerebral Hemodynamics CBF-cerebral blood flow CPP- cerebral perfusion pressure CBV- cerebral blood volume Cerebral oxygenation All need to maintained for normal brain function
15
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
16
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.
17
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
18
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
19
Alterations in Movement Abnormal movements occur in CNS dysfunctions alter nerve innervations. Paresis- ( weakness ) partial paralysis Paralysis- loss of motor function
20
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
21
Alterations in Movement
22
Lower Motor Neuron Syndromes
23
Amyotrophies- ALS –Paralytic poliomyelitis –Nuclear palsies –Progressive spinal muscular atrophy –Progressive bulbar palsy –Bulbar palsy
24
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
25
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)
26
Alterations in Movement Hypokinesia –Decreased movement –Akinesia- loss of voluntary movements due to loss of dopamine –Bradykinesia –Loss of associated movement
27
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
28
Parkinson Disease
29
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
30
Disorders of Posture (Stance)
31
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
32
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
33
Disorders of Expression
34
Extrapyramidal Motor Syndromes Basal ganglia motor syndromes Cerebellar motor syndromes Both result in movement or postural disturbances without significant paralysis
Similar presentations
© 2024 SlidePlayer.com Inc.
All rights reserved.