Patho-Neurology

Chronic, progressive failure of many cerebral functions including impairment of intellectual processes

loss of orientation, memory, language, judgement, decision making, behavior

not a disease, group of symptoms caused by brain damage

dementia-defined

neuron degeneration (no repair)

brain compression

atherosclerosis of cerebral vessels (plaque in brain)

brain trauma (athletes)

CNS infections & neuroinflammation (alcoholic)

dementia-pathophysiology

progressive neurological deterioration & continuing decline affecting memory, thinking skills, inability to carry out simplest tasks

most common type in older people

key factor=increase in age

LATE ONSET(non-hereditary) 60-80yrs & MOST COMMON

EARLY ONSET 30-50yrs/familial-autosomal dominant/ non-familial-down syndrome

alzheimer’s - defined

extracellular-deposition of beta-amyloid (plaque)

intracellular-accumulation of tau proteins(tangles)

degeneration of basal forebrain cholinergic neurons-loss of acetylcholine

alzheimer’s-pathophysiology

early symptoms-forgetfulness (short term memory), emotional upset

later symptoms-memory loss, disorientation, confusion, disorientation, lack of concentration, decline in problem solving

progressive:10-20yrs

alzheimer’s-signs & symptoms

no specific treatment

anticholinesterase drug-temporary (cholinesterase kills acetylcholine)

team approach needed to support patients & caregivers

treat symptoms, not cure

alzheimer’s-treatment

progressive, neurodegenerative disease of the basal ganglia with the loss of dopamine-providing neurons

hypokinetic movement

parkinson’s disease

intraneuronal Lewy Bodies inclusions composed of α-synuclein

Types: Primary: idiopathic-most common, 60-80yrs/ genetic association

Secondary: environmental-pesticides/herbicides

anti-psychotic meds

pseudo-parkinsonism (Muhammed Ali)

parkinson’s-pathogenesis

masked facies | stooped posture

rigidity | slow movement

poor balance | short shuffling steps

tremors

parkinson’s-signs & symptoms

levodopa-dopamine replacement therapy

anticholinergic drugs (blocks parasympathetic)- stops shakes

amantadine- decrease tremors

team approach-speech & language pathologist | physical & occupational therapy

monitoring & treatment of respiratory & UTIs

parkinson’s-treatment

progressive, debilitating neurodegenerative inherited disease

autosomal dominant Gg

doesn’t manifest until around 40yrs old

huntington’s

hyperkinetic disorder (artistic arm movement)

depletion of gamma-aminobutyric acid (GABA)- inhibitor

levels of acetylcholine in the brain appear to be reduced

results in progressive atrophy of the brain

huntington’s-pathophysiology

mood swings | personality changes

restlessness

choreiform (purposeless) movements w/out conscious effort

emotional changes

huntington’s-signs & symptoms

DNA analysis because it’s inherited lol

huntington’s- diagnosis

no specific treatment | treat symptoms only

mortality: suicide | infection | heart disease

huntington’s- treatment

rapidly progressive & fatal neurodegenerative disease of the upper & lower motor neurons

AKA Lou Gehrig’s disease

no indication of inflammation around the nerves

cognition impaired

amyotrophic lateral sclerosis ALS- defined

SOD I gene mutation - most common

military vets - Gulf War

risk-repeated trauma (athletes) - Lou Gehrig

amyotrophic lateral sclerosis ALS- pathogenesis

spastic paralysis-loss of upper motor neurons

flaccid paralysis-loss of lower motor neurons

progressive muscle weakness & loss of fine motor skills (stumbling & falls common)

death from respiratory failure

amyotrophic lateral sclerosis ALS- pathophysiology

limb cramping or weakness

similar to stroke- incoordination | slurring of speech | dysphagia-difficulty swallowing

single group paresis (muscle weakness) that spreads

hypotonia-muscle tone loss( ya insides)

survival: 3-5yrs from diagnosis

amyotrophic lateral sclerosis ALS- clinical manifestations

maintain quality of life | involve family in treatment

not much you can do because ya fucked

amyotrophic lateral sclerosis ALS- treatment

frequently occurring neurological disorders caused by pathologic processes in the blood vessels

cerebrovascular disease

ischemia (low blood flow)

hemorrhagic (balloon pop) - increased intracranial pressure

vascular malformation

cerebrovascular disease- pathogenesis

transient ischemic attacks (TIAS)

cerebral vascular accident (CVA {stroke}):

thrombotic-deep vein thrombosis

embolic- bone marrow goes to heart | amniotic fluid | O₂ pocket

hemorrhagic- blood bleeds out

cerebrovascular disease- types

transient episode of neurologic dysfunction by focal brain, spinal cord, or retinal ischemia w/out acute infarction

acute- lasting less than an hour from ischemic event

reversible

transient ischemic attacks TIAS

atherosclerosis- most common

small embolus- blockage

vascular spasms- constriction

arteritis- artery inflammation

mass lesions- cancer

transient ischemic attacks TIAS- causes

difficult to diagnose after attack

directly located to location of ischemia

intermittent short episodes of impaired function

muscle weakness in arm of leg

visual disturbances

numbness & paresthesia (pins & needles)

transient aphasia (language disorder)

goes away & is a warning sign

transient ischemic attacks TIAS- signs & symptoms

rule out other causes

baseline bloodwork

MRI- preferred | CT scan

carotid doppler

angiography

transient ischemic attacks TIAS- diagnosis

risk stratification

start stroke prevention therapy

transient ischemic attacks TIAS- management

an infarction (tissue death by lack of blood flow) - hypoperfusion

leading cause of disability

african american-higher risk

cerebrovascular accidents CVAs- defined

ischemic- occlusion of blood vessel by a thrombus of embolus

hemorrhagic- rupture of cerebral vessel-hypertension

cerebrovascular accidents CVAs- classifications

hypertension- most common cause

bleeding→ compressed brain tissue→ ischemia, edema, ICP & necrosis

bleeding types: intracerebral | subarachnoid

cerebrovascular accidents CVAs- hemorrhagic stroke

non-modifiable factors

modifiable factors- hypertension, diabetes, smoking, sedentary lifestyle

cerebrovascular accidents CVAs- risk factors

lack of voluntary movement or sensation on the opposite side of body

initially flaccid paralysis → then becomes spastic later on

cerebrovascular accidents CVAs- signs & symptoms

focused on restoration of perfusion, countering ischemia, preventing necrosis

surgery: endarectomy- embolic & ischemic stroke | clot removal/clamp bleeding- hemorrhagic

aspirin | systemic anticoagulation | thrombolysis | anti-platelet therapy & statins | blood pressure control | glucocorticoids- minimizes brain swelling | underlying problems | immediate rehab

cerebrovascular accidents CVAs- treatments

aspirin- platelet antiaggregant

statins- cholesterol lowering drugs

control hypertension | control diabetes type II | stop smoking “cessation” | lifestyle changes

cerebrovascular accidents CVAs- prevention

inflammation & infection of the membrane covering the brain & spinal cord- dura mater, arachnoid mater, subarachnoid, pia mater

meningitis

bacteria-most severe (will fucking kill you) | N meningitidis gram- | S pneumonia gram +

viral (aseptic)- most common, not deadly (meds, autoimmune, cancer)

fungal- associated w/suppressed immune system (last of us)

meningitis- etiology

microorganisms reach the brain via: blood & nearby bordering tissue

infections spread rapidly through meninges

inflammatory response leads to increased intracranial pressure

exudate (pus) present in the cerebrospinal fluid

meningitis- pathophysiology

elicits pain or limited extension

hip & knee at 90°

Kernig sign

elicits hip & knee flexion

passive flexion of neck

Brudzinski sign

rapid diagnosis & treatments to prevent morbidity & mortality

identify organism that’s fucking you up

aggressive antimicrobial therapy

glucocorticoids- reduces swelling

vaccines available

meningitis- treatments

chronic progressive immune-mediated inflammatory disease w/ progressive demyelination of neurons in the CNS; brain, spinal cord, cranial nerves

targets oligodendrocytes

autoimmune

white people shit- mostly women

relapses/remission can happen- becomes irreversible over time

multiple sclerosis MS

Lhermitte sign

jolt in back- MS

paresthesia (pins & needles) | double vision

poor coordination | sensory deficits

loss of bowel & bladder control | memory loss

multiple sclerosis MS- clinical manifestations

full neurological exam | no specific marker

MRI- diagnosis & monitoring | CSF analysis

multiple sclerosis MS- diagnostics

no definitive treatment | corticosteroids

immunotherapy- transfusions | vitamin D

physical & occupational therapy

multiple sclerosis MS- treatment