Week three notes

Mosby items and derived items © 2012 Mosby, Inc., an imprint of Elsevier Inc. 11

Alterations in Cognitive Systems, Cerebral Hemodynamics and

Motor Function


Alterations in Cognitive Systems

Consciousness State of awareness of oneself and the

environment Arousal

• State of awakeness


Alterations in Arousal

Structural Divided by location above or below tentorial

plate Metabolic Psychogenic


Alterations in Arousal (cont’d)

Coma is produced by either: Bilateral hemisphere damage or suppression Brain stem lesions or metabolic derangement

that damages or suppresses the reticular activating system


Alterations in Arousal

Clinical manifestations: Level of consciousness changes Pattern of breathing

• Posthyperventilation apnea (PHVA)• Cheyne-Stokes respirations (CSR)

Pupillary changes Oculomotor responses Motor responses Vomiting, yawning, hiccups


Clinical Manifestations


Clinical Manifestations (cont’d)






Brain Death (Total Brain Death)

Body can no longer maintain internal homeostasis

Brain death criteria: Completion of all appropriate and therapeutic

procedures Unresponsive coma (absence of motor and

reflex responses) No spontaneous respirations (apnea)


Brain Death (Brain Stem Death)

Brain death criteria: No ocular responses Isoelectric EEG Persistence 6 to 12 hours after onset


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


Cerebral Death (cont’d)

Survivors of cerebral death: Remain in coma Emerge into a persistent vegetative state Progress into a minimal conscious state (MCS) Locked-in syndrome


Alterations in Awareness

Selective attention: Ability to select from available, competing

environmental and internal stimuli Sensory inattentiveness

• Extinction• Neglect syndrome

Selective attention deficit


Alterations in Awareness (cont’d)

Memory Amnesia

Retrograde amnesia Anterograde amnesia Executive attention deficits

• ADHD Image processing


Seizures

Syndrome versus disease Sudden, transient alteration of brain

function caused by an abrupt explosive, disorderly discharge of cerebral neurons

Motor, sensory, autonomic, or psychic signs


Seizures (cont’d)

Convulsion Tonic-clonic (jerky, contract-relax) movements

associated with some seizures Epilepsy: no underlying cause can be

found


Seizures (cont’d)

Etiologic factors: Cerebral lesions Biochemical disorders Cerebral trauma Epilepsy


Seizures (cont’d)

Partial seizures Simple, complex, secondary generalized

Generalized seizures Absent, myoclonic, clonic, tonic-clonic, atonic

Unclassified epileptic seizure


Seizures (cont’d)

Aura Prodroma Tonic phase

Contraction Clonic phase

Relaxation Postictal phase


Data Processing Deficits

Agnosia Tactile, visual, auditory, etc.

Dysphasia Expressive dysphasia Receptive dysphasia Transcortical dysphasia

Aphasia


Acute Confusional States (ACS)

Transient disorders of awareness that result from cerebral dysfunction Secondary to drug intoxication, metabolic

disorder, or nervous system disease Delerium

• Hyperkinetic• Hypokinetic


Dementia

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

Losses: Orientation Memory Language Judgment Decision making


Alzheimer Disease (AD)

Familial, early and late onset Nonhereditary (sporadic, late onset) Theories:

Mutation for encoding amyloid precursor protein

Alteration in apolipoprotein E Loss of neurotransmitter stimulation of choline

acetyltransferase


Alzheimer Disease (AD) (cont’d)

Neurofibrillary tangles Senile plaques 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 CPP CBV Cerebral oxygenation


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


Herniation Syndromes

Supratentorial herniation Uncal

• Uncus or hippocampal gyrus (or both) shifts from the middle fossa through the tentorial notch into the posterior fossa

Central• Downward shift of the diencephalon through the

tentorial notch Cingulate

• Cingulate gyrus shifts under the falx cerebri


Herniation Syndromes (cont’d)

Infratentorial herniation Cerebellar tonsil shifts through foramen

magnum


Cerebral Edema

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

Types: Vasogenic Cytotoxic Interstitial


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


Hydrocephalus (cont’d)

Noncommunicating hydrocephalus Internal Intraventricular

Communicating (extraventricular) hydrocephalus

Acute hydrocephalus Normal-pressure hydrocephalus


Alterations in Neuromuscular Function

Muscle tone Hypotonia Hypertonia

• Spasticity• Gegenhalten (paratonia)• Dystonia• Rigidity


Alterations in Movement

Paresis and paralysis Upper motor neuron syndromes:

• Hemiparesis or hemiplegia• Diplegia• Paraparesis or paraplegia• Quadriparesis or quadriplegia• Pyramidal motor syndromes• Spinal shock


Alterations in Movement (cont’d)





Lower motor neuron syndromes: Flaccid paresis or flaccid paralysis Hyporeflexia or areflexia Fibrillation


Lower Motor Neuron Syndromes


Lower Motor Neuron Syndromes (cont’d)

Amyotrophies: Paralytic poliomyelitis Nuclear palsies Guillain-Barré syndrome 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 Tardive dyskinesia



Huntington disease Also known as chorea Autosomal dominant hereditary degenerative

disorder Severe degeneration of the basal ganglia

(caudate nucleus) and frontal cerebral atrophy• Depletion of gamma-aminobutyric acid (GABA)



Hypokinesia Decreased movement Akinesia Bradykinesia Loss of associated movement


Parkinson Disease

Severe degeneration of the basal ganglia (corpus striatum) involving the dopaminergic nigrostriatal pathway Parkinsonian tremor, rigidity, bradykinesia Postural disturbances Autonomic and neuroendocrine symptoms Cognitive-affective symptoms

Secondary parkinsonism


Disorders of Posture (Stance)

Dystonia Dystonic postures and movements Decorticate posture Decerebrate posture Basal ganglion posture Senile posture


Disorders of Posture (Stance) (cont’d)


Disorders of Gait

Spastic gait Scissors gait Cerebellar gait Basal ganglion gait Senile gait


Disorders of Expression

Hypermimesis Hypomimesis Dyspraxias and apraxias


Disorders of Expression (cont’d)


Extrapyramidal Motor Syndromes

Basal ganglia motor syndromes Cerebellar motor syndromes


Alterations of Neurologic Function in Children


Review

Remember there are many differences in the nervous system with children:

Do you remember the following:

*Fontanels *Sutures *Reflexes

We Will explore one major area in children, in this weeks notes


Childhood Brain Tumors

Brain tumors: Medulloblastoma Ependymoma Cerebellar astrocytoma Brain stem glioma

• Craniopharyngioma Optic glioma


Childhood Brain Tumors

Health & Medicine

Week three notes