Concepts of Neurologic Dysfunction

7/31/2019 Concepts of Neurologic Dysfunction

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Chapter 14


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Level of Consciousness the most critical clinical index of

nervous system function, with

changes indicating eitherimprovement or deterioration ofthe individuals condition

Table 14-3 Levels of Altered Consciousness


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Alterations in Cognitive Networks

Full consciousness: awareness of self and theenvironment

Arousal: state of awakeness

Mediated by the reticular activating systemContent of Thought: all cognitive functions

Awareness of self, environment and affectiv

states (moods)


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Alterations in Arousal

Causes Table 14-1 & 14-2Structural

Divided by location above or below

tentorial plateMetabolic

Psychogenic


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Alterations in Arousalrange from slight drowsiness to coma

Comaproduced by either Bilateral cerebral hemisphere damage or

suppression Brain stem* lesions or metabolic derangement that

damages and suppresses the reticular activatingsystem

*midbrain, medulla, pons (Figure 12-5)


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Alterations in Arousal Clinical manifestations : critical for evaluation

extent of brain dysfunction

index for identifying or CNS function

1) Level of consciousness

2) Pattern of breathing

- Post hyperventilation apnea (PHVA)

- CheyneStokes respiration (CSR)

3) Pupillary changes (size and reactivity)

4) Oculomotor response (position andreflexes)

5) Motor response (skeletal muscle)


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President Lincoln April 14, 1865


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Pathway of the bullet


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Clinical Manifestations


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Decorticate & Decerebrate


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Brain Deathnever recover nor maintain internal

homeostasis

Total Brain Death criteria (5):

(cerebrum, brain stem & cerebellum)

Completion of all appropriate and

therapeutic proceduresUnresponsive coma (absence of motor

and reflex responses)

No spontaneous respirations (apnea)


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Cerebral Deathdeath exclusiveofbrain stem and

cerebellum

No behavioral or environmental responses Brain continues to maintain internal

homeostasis

Survivors Coma Vegetative state (wakeful unconscious state)

Minimal conscious state

Locked-in syndrome


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Seizures Sudden, transient alteration of brain function

caused by an abrupt explosive disorderlydischarge of cerebral neurons

Alteration in brain function (transient)

Altered level of arousal

Convulsion seizure with tonic-clonic movement

Epilepsy seizures recur without treatment (5 to

10/1000)


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Conditions - Seizures Cerebral lesions

Biochemical disorders

Cerebral trauma

Epilepsy


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Seizures Partial (focal/local)

Simple, complex, secondary, generalized

Generalized (bilateral/symmetric)

Unclassified


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Seizures

Epileptogenic focus

Group of neurons that appear to behypersensitive to sudden depolarization

Hyperthermia, hypoxia, hypoglycemia,hyponatremia, sensory stimulation and certainsleep phases

Aura partial seizure precedes generalized

Prodroma early manifestation hours to days

before


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Seizures Tonic contraction

Excitation spreads to subcortical, thalamic andbrain stem areas

Loss of consciousness

Clonic relaxation

Inhibitory neurons of cortex, anterior thalamusand basal ganglia


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Alterations in Awareness

Memory Retrograde amnesia past memories

Antegradeamnesia new memories

Temporary or permanent(severe head injury orAlzheimer disease)

Executive attention deficits

Inability to maintain sustained attention

Inability to set goals Working memory deficit

Table 14-6 Clinical manifestations


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Memories:amygdala hippocampus

thalamus prefrontal cortex


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Data Processing Deficits

Agnosiafailure to recognize the form andnature of an object: CVA

Tactile, visual, auditory

Dysphasiainability to arrange words inlogical order: CVA (middle cerebral artery-Lcerebral hemisphere)

Expressive cannot find words, difficulty writing(Brocas area)

Receptive language is meaningless (inappropriate

words, neologisms) Wernicke


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Data Processing Deficits

Dementia* Progressive failure of cerebral functions that is not

caused by an impaired level of consciousness

orienting, memory language and executiveattention networks

Table 14-13 Comparison of Delirium & Dementia


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Dementia Degeneration of neurons

Compression-space occupying lesion

Atherosclerosis

Genes-Alzheimer & Huntington diseases

CNS infection HIV, Creutzfeldt-Jakob

nerve cell damage and brain atrophy


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Alzheimer Disease (AD)

Familial onset

Early-onset-chromo mutations # 21 (very rare)

Late onset-90% cases ? Chromo #19*

Theories

Mutation for encoding amyloid precursor protein

Alteration in apolipoprotein E*

Loss of neurotransmitter of choline


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Alzheimer Disease (AD)

Neurofibrillary tangles

Senile plaques

Clinical manifestations

Forgetfulness, emotional upset, disorientation,confusion, lack of concentration, decline in abstraction,problem solving and judgment

Diagnosis R/O other causes


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Burden of Alzheimers Disease 5.4 million Americans 16 million by 2050

6th leading cause of death:#prevented, cured, slowed

>/= 65y/o average survival: 4-8 yrs, may up to 20yrs Caregivers burden: 60% emotional stress

:30%depressed

Cost 2011: $183 billion $1 trillion by2050

J.Alzheimers Assoc. March 2011


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Know the Signs Memory loss that disrupts daily life

Trouble planning or solving problems

Difficulty completing tasks Confusion with time or place

Trouble understanding images and spatialrelationships

New problems with speaking or writing words Misplacing things and inability to retrace steps

Decreased or poor judgment


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Know the Signs Social withdrawal

Change in mood or personality

Review Table 14-14


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Cerebral Hemodynamics

CBF blood flow

CPP perfusion pressure

CBV blood volume

Cerebral oxygenation

critical factor


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Injury States cerebral perfusion

Normal perfusion but intracranial pressure(ICP)

cerebral blood volume

SO: must maintain CPP and control ICP


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Increased Intracranial Pressure(IICP)

intracranial content, edema, excess CSF orhemorrhage

Normal 5 to 15 mmHg

Stages 1-4 (Figure 14-10)

Stage 1 vasoconstriction and external compressionof venous system - ICP (autoregulation)

Stage 2


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General

Autoregulation - blood vessel diameterto maintain a constant blood flow is lost with ICP

vasoconstriction to elevate BP > ICP

a) O2CO2 deteriorationb) small pupils, neurologic hyperventilation, widened

pulse pressure and HR

Local vasodilation 2 to CO2

BV ICP approaches SBP - perfusion with severehypoxia/acidosis

IICP not evenly distributed throughout the

cranial vault


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Cerebral Edema Increase in the fluid (intracellular or extracellular)

within the brain ( volume)

Results: trauma, infection, hemorrhage, tumor,

ischemia, infarct or hypoxia

1)Vasogenic: BBB is disrupted - plasma protein toextracellular space - ICP

2)Cytotoxic: toxic factors failure NA-K+ transportsystem: K+ out, H2O in

3)Ischemic (infarction): vasogenic and cytotoxic cellnecrosis lysosomes BBB

4)Interstitial (hydrocephalus): volume about ventricles


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Hydrocephalus (Types Table

14-16) Excess fluid within the cranial vault,

subarachnoid space or both

Caused by interference in CSF flow

reaborption

fluid production

Obstruction

Infancy through adulthood


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Spinal Shockcomplete cessation of spinal cord function belowthe lesion

Complete flaccid paralysis

Absence of reflexes

Marked disturbance of bowel and bladder function

Days to weeks

Return of spinal reflexes hyperactive

spasticity, rigidity


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Michael J Fox


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Parkinson DiseaseAfter age 40 peak onset 58 62 years

107 to 187 per 100,000

Severe degeneration of the basal ganglia involving

dopaminergic nigrostriatal pathway Dopamine: inhibitory neurotransmitter

Acetylcholine: stimulatory neurotransmitter

IMBALANCEof neurotransmitters motormodulation

Ach________________Dopamine


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Parkinson Disease


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Parkinson Disease Clinical manifestations

Tremor at rest

Rigidity (muscle stiffness)

Bradykinesia (poverty of movement)

Postural disturbance Dysarthria (uttering of words)

Dysphagia (difficulty swallowing)

Progressive dementia


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Concepts of Neurologic Dysfunction

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