Ch 16, 17, And 18 High Patho

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3 major neural systems accounting for functional adequacy:

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1. cognitive systems
2. sensory systems
3. motor systems

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AD is associated with ?

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Down's syndrome

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neurofibrillary tangle

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an insoluble helical formation formed when Tau protein detaches from microtubule

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where plaques and tangles are most prevalent in AD

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cerebral cortex and hippocampus

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when is AD associated with more dysfunction?

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when number of plaques and tangles is greater

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what causes ICP?

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increased intracranial content
edema
excess CSF
hemorrhage

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rise in ICP results in ?

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equal volume reduction of other contents

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what is usually displaced when there is ICP?

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CSF

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Stage 1 ICP

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cerebral blood volume is altered; vasoconstriction try to decrease pressure; ICP ma not change because of compensatory mechanism

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Stage 2 ICP

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pressure begins to compromise neuronal oxygenation and arterial vasoconstriction occurs to elevate pressure

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what happens as ICP begins to approach arterial pressure?

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brain tissues begin to experience hypoxia and hypercapnia; condition deteriorates rapidly

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Stage 3 ICP

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autoregulation is lost, accumulating CO2 may cause vasodilation and now causes blood pressure in vessles to drop and blood volume to increase; pressure continues to rise

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Stage 4 ICP

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brain tissues herniate from compartment of greater pressure to compartment of lower pressure causing further hypoxia and ischemia

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types of herniation syndromes

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supratentorial herniations
infratentorial herniation

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types of supratentorial herniations

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1. uncal
2. central (transtentorial)
3. cingulate gyrus

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uncal hernation

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occurs when the uncus or hippocampal gyrus shifts from middle fossa through the tentorial notch into the posterior fossa

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what causes uncal herniation?

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an expanding mass in lateral region of middle fossa

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central herniation

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straight downward shift of diencephalon through the tentorial notch

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what causes central herniation?

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injuries or masses located around outer perimeter of frontal, parietal, or occipital lobes; extracerebral injuries around central apex of the cranium; bilatterally position injuries or masses; unilateral cinguate gyrus herniation

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cingulate gyrus herniation

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when the cingulate gyrus shifts under the falx cerebri

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cerebral edema

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increase in the fluid content of brain tissue

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when does this occur?

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can occur from a result from trauma, infection, hemorrhage, tumor, ischemia, infarct, or hypoxia

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4 types of cerebral edema

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1. vasogenic
2. cytoxic
3. ischemic edema
4. interstitial

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vasogenic edema

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most important; caused by increased permeability of the capillary endothelium of the brain after injury to the vascular structure; results in disruption of blood-brain barrier

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where does vasogenic edema start and where does it spread?

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starts in area of injury
spreads with preferential accumulation in the white matter of the ipsilateral side

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cytoxic edema

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toxic factors directly affect the cellular elements of the brain parencyma, causing failure of the active transport systems

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where does cytoxic edema occur

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primarily in gray matter

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ischemic edema

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follows cerebral infarction

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interstitial edema

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caused by transependymal movement of CSF from the ventricles into the extracellular spaces of the brain tissues

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where does HD occur?

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basal ganglia and cerebral cortex

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onset of HD

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30-50 y/o

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inherited/non-inherited HD

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inherited

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dominant or recessive HD

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autosommal dominant; repeated trinucleotide (CAG)

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principal biochemical alteration in HD

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basal ganglia and nigral depletion of GABA

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decreased GABA causes what to happen in HD

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increase in dopaminergic acitivty

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motor clinical manefestations of HD

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choreiform movements begin in face and arms, then to entire body

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hypokinesia

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loss of voluntary movement despite preseved consciousness and normal peripheral nerve and muscle function

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akinesia

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absence, poverty, or lack of control of associated and voluntary muscle movements; dysfunction of the extrapyramidal system (deficiency of dopamine)

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bradykinesia

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slowness of voluntary movements; difficulty initiating movements, continuing movements, performing synchronous and consecutive tasks

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loss of associated movement

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finely tuned movements which provide grace,skill, and balance; loss of facial expression and gestures

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where does Parkinsons occur?

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basal ganglia (corpus striatum) involving dopaminergic nigrostriatal pathway

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onset of parkinsons

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after 40 years of age

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autosomal dominant form of Parkinsons

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mutation in alpha synuclein gene on chromosome 4

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autosomal recessive form of Parkinsons

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mutation in the parkin gene or chromosome 6

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classification of Parkinsonian syndromes

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1. Idiopathic Parkinson disease
2. Symptomatic parkinsonism
3. as part of a neuronal degenerate disorder

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symptom developments result from ? in parkinsons

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imbalance of dopaminergic and cholinergic activity in the caudate nucleus and putamen of basal ganglia

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parkinsonian tremor

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1st symptom; asymmetric, regular, rhythmic, low-amplitude tremor; tremor stops during voluntary movement

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Parkinsonian rigidity

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state of involuntary contraction of all skeletal muscles, impedes active and passive movement

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Parkinsonian bradykinesia

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loss of associated and voluntary movements (all striated muscles); difficulty chewing, swallowing, and articulating

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hypokinesia

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decreased frequency or absence of associated movements

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postural abnormalities

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postural fixation, equilibrium, postural righting

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autonomic and neuroendocrine symptoms of parkinsons

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inappropriate diaphoresis, orthostatic hypotension, gastric retention, constipation, urinary retention

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cognitive-effect symptoms of parkinsons

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endogenous depression, disorientation, confusion, memory loss, distractibility, difficutly with concept formaiton, abstraction, calculations, thinking, judment

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treatment for Parkinsons

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dopaminergic drugs:
- levodopa, dopamine agonists, anticholinergic drugs, antihistamines, amantadine

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categories of brain injuries

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blunt trauma
open trauma

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focal brain injuries

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contusions, epidural hemorrhage, subdural hematoma, intracerebral hematoma

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primary injury

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caused by the impact and involves neural injury, primary glial injury, and vascular response

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secondary injury

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cerebral edema, brain swelling, hemorrhage, infection, increased ICP; hypoxia from cerebral ischemia

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tertiary injury

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caused by apnea, hypotension, change in pulmonary resistance, change in EEG (ST and T wave changes)

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mild concussion

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temporary axonal disturbances; confusion and loss of memory

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Grade I conussion

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momentary amnesia

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Grade II concussion

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retrograde amnesia that develops after 5 to 10 minutes

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Grade III concussion

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confusion and retrograde amnesia present from impact

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Grade IV classic cerebral concussion

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immediate loss of consciousness lasting less than 6 hours w/retrograde and anterograde amnesia

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diffuse axonal injury

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mild, moderate, or severe

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mild DAI

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coma lasting 6-24 hrs; deficits may persist

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moderate DAI

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actual tearing of some axons in both hemispheres, coma last 24 hrs +, incomplete recovery in 93% that survive

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severe DAI

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64% survive, 30-40% stay at a low level or reduced state of consciousness for a prolonged period of time

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Ischemic strokes

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white strokes

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hemorrhagic strokes

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red strokes - bleeding into brain

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risk factors for stroke

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hypertension
smoking
diabetes
insulin resistance
polycythemia
thrombocythemia
elevated lipoprotein-a
impaired cardiac function
hyperhomocysteinemia
nonrheumatic atrial fibrillation
Chlamydia pneumonia infection

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meningitis

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infection of meninges

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causes of meningities

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bacteria, viruses, fungi, parasites, other toxins

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bacterial meningitis

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infection of pia mater and arachnoid, subarachnoid space, ventricular system, CSF

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common causes of bacterial meningitis

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Miningococcus and pneumococcus

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aseptic meningitis (viral)

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inflammation limited to the meninges

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fungal meningitis

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chronic, much less common condition

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who is usually infected by fungal meningitis

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people with impaired immune responses or alteration in normal body flora

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tubercular meningitis

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most common and serious form of CNS tuberculosis

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abscess

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localized collections of pus within the parenchyma of the brain and spinal cord

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when do abscess occur?

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after open trauma or neurosurgery
in association with a contiguous focus of infection
through metastatic or hematogenous spread from distant folci
cryptogenically

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most common site for abscesses?

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frontal and temporal lobes

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4 stages of brain abscess

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1. early cerebritis
2. late cerebritis
3. early capsule formaiton
4. late capsule formation

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early cerebritis

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localized inflammatory process where inflammatory cells surround a central core of coagulative necrosis; marked cerebral edema

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late cerebritis

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necrotic center is surrounded by inflammatory infiltrate of macrophages and fibroblasts, new blood vessel formation around abscess, still cerebral edema

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early capsule formation

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necrotic center decreases in size, mature collagen evolves forming capsule

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late capsule formation

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well formed necrotic center surrounded by a dense collagenous capsule

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3 layers of mature abscess

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1. center of polymorphonuclear leukocytes
2. collagenous capsule
3. peripheral gliosis

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encephalitis

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an acute febrile illness, usually of viral origin, with nervous system involvement

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most common cause of encephalitis

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arthropod-borne viruses and herpes simplex I in adults

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Multiple sclerosis

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relatively common dysimmune disorder diffusely involving CNS myelin

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MS primary or secondary?

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primary demyelinating disorder

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3 purposes of MS treatment

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1. acute management of relapses to prevent disability
2. reducing frequency of relapses and/or minimizing disease progression
3. management of symptoms

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3 classifications of neuropathies

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1. generalized symmetric polyneuropathies
2. generalize neuropathies
3. focal or multifocal neuropathies

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generalize symmetric polyneuropathies

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characterized by symmetric involvement of sensory, motor, or autonomic fibers; one type of fiber might dominate

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generalized neuropathies

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affect the cell body of only one type of peripheral neuron

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focal or multifocal neuropathies

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affect sensory and motor fibers in one or more nerves as is seen in common compression neuropathies such as carpal tunnel

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ALS

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degenerative disorder diffusely involving lower and upper motor neurons resulting in progressive muscle weakness leading to respiratory failure and death usually 2 to 5 years form symptom onset

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clinical manifestations of ALS

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1. paresis beginning in single muscle group
2. muscle groups asymmetrically affected
3. gradual involvement occurs in all striated muscles except extraocular muscles and heart and progresses to paralysis
4. flaccid and spastic paresis may coexist in a single muscle group
5. urethral and anal sphincter weakness
6. no associated mental, sensory, or autonomic symptoms

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radiculopathies

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disorders of roots of spinal nerves

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possible causes of radiculopathies

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tearing of a nerve, compression of a nerve, chronic meningitis, neurosyphilis, sarcoidosis, etc.

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myasthenia gravis

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a chronic autoimmune disease mediated by antiacetylcholine receptor antibodies (IgE) that act at the neuromuscular junction

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characteristics of MG

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exertional fatigue and weakness that worsens with activity, improves with rest, and recurs with resumption of acitivty

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neonatal MS

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onset of signs 1-3 days after birth and persist for a few days to a few weeks

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congenital MS

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presents in infancy and continues onto adulthood

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Venile MS

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autoimmune disorder with a childhood onset usually about 10 years of age

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ocular MG

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involves muscle weakness of the eye muscles and eyelids and may include swallowing difficulties and slurred speech

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generalize autoimmune MG

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involves proximal musculature throughout the body and has several courses