Neurological Disorders Flashcards
Dementia
Not a specific disease – group of
symptoms caused by brain
damage
- Progressive
Loss of cognitive functioning
(thinking, remembering, reasoning)
Interferes with daily activities
Occurs in older people
Not a normal aging process
Dementia Mechanisms
◦Neuron degeneration
◦Atherosclerosis/vascular
◦Brain tissue compression
◦Brain trauma
◦Genetic predisposition
Alzheimer
Disease
Progressive neurological
disorder effecting memory,
thinking skills, the inability to
carry out simplest tasks
MOST COMMON type of DEMENTIA
Late onset (95%)
Sporadic
Alteration in apolipoprotein E
(chromosome 19)
Early-onset familial (5%)
Chromosome 21
Alzheimer
Disease Pathophysiology
Extracellular deposition of β-amyloid
Senile (neuritic) plaques
Intracellular accumulation of tau protein
Neurofibrillary tangles
Alzheimer
Disease Signs and symptoms
◦ Extend over 10 to 20 years
◦ Behavioral changes
◦ Irritability, hostility, mood
swings
◦ Forgetfulness ->
progressive memory loss
◦ Lack of concentration
◦ Impaired learning or use of
language
◦ Poor judgment
Alzheimer’s
Disease Diagnostics
No definite clinical diagnostic tests
Confirm – postmortem brain biopsy
Exclusion of other disorders
Careful medical and psychological
history
Treatment
No specific treatment
Anticholinesterase drugs
* Temporary improvement
Team approach needed to support
patients and caregivers
Occupational, speech, physical,
psychologists
Parkinson’s Disease
Progressive, neurodegenerative disease of the melanin-containing dopaminergic neurons in
the substantia nigra, pars compacta
Severe degeneration of the basal ganglia
Parkinson’s Types
Types
Primary – (Idiopathic) - majority
Secondary
Environmental
(pesticides/herbicides)
Anti-psychotic medications
Pseudo-Parkinsonism -
Muhammad Ali
Parkinson’s
Disease Treatments
- Dopamine agonist
- Levodopa
- MAO-B inhibitor
- Anticholinergic drugs
- Amantadine
- Team approach
- Speech, physical, exercise
therapy - Psychiatric comorbidities
- Dietary
Huntington’s Disease
Progressively debilitating
neurodegenerative inherited
disease
Autosomal dominant disorder
Chromosome 4 (4p16.3)
Huntingtin (HTT) gene
Signaling, transporting, anti-
apoptosis, DNA repair
Does not usually manifest until
older ~ 40s
Progressive atrophy of brain
Huntington’s Pathophysiology
Pathophysiology
- Hyperkinetic disorder
- Involves basal ganglia (nuclei) and frontal cortex
- Depletion of gamma-aminobutyric acid (GABA) in the
basal nuclei (caudate nucleus & putamen)
- Levels of acetylcholine in brain appear to be reduced
Huntington’s Disease Signs and symptoms
◦ Mood swings, personality
changes
◦ Restlessness, choreiform
(purposeless) movements in
arms and face
Huntington’s Diagnostics
DNA analysis
Huntington’s Treatment
◦ Currently no specific
treatment
◦ Symptomatic therapy only
Huntington’s Mortality
◦ Infection
◦ Heart disease
◦ Suicide
Amyotrophic Lateral Sclerosis
(ALS)
Also referred to as Lou Gehrig’s disease
Rapidly progressive & fatal
neurodegenerative disease of the upper
and lower motor neurons
Pathophysiology: not clear
SOD1 gene mutation
Damage to glutamate uptake channels in
astrocytes
Military veteran – Gulf War
Risk - repeated trauma (athletes)
No indication of inflammation around the
nerves
Cognition and sensory: UNIMPAIRED
Amyotrophic Lateral Sclerosis [2]
Loss of upper motor neurons
Spastic paralysis & hyperreflexia
Damage to lower motor neurons
Flaccid paralysis and hyporeflexia
Progressive muscle weakness
Loss of fine motor coordination
Stumbling and falls are common.
Death due to respiratory failure
Vascular
Disorders
Ischemia - interference with
blood supply
- Damage and manifestations
depend on cerebral artery
involved
- Global or local
Hemorrhage
- Increased intracranial
pressure (ICP) will cause
local ischemia and
generalized symptoms.
Vascular malformations
- Arteriovenous malformation
Cerebrovascular
Disorders
Transient ischemic attacks
(TIAs)
Cerebral vascular accident
(CVA [stroke])
+ Thrombotic stroke
- Arterial occlusions caused by
thrombi
+ Embolic stroke
- Fragments of a thrombus that
broken free from a thrombus
Hemorrhagic stroke
Transient
Ischemic
Attacks
(TIAs)
Transient episode of neurologic dysfunction caused by focal brain, spinal cord, or retinal ischemia without acute infarction
Neurological dysfunction lasting <1
hour from ischemic event
Reversible
Causes
- Atherosclerosis – most common
- Partial occlusion of an artery - small embolus
- Vascular spasm
- Arteritis
- Mass lesions
Transient
Ischemic
Attacks S&S
Signs and symptoms
Difficult to diagnose after the
attack
Directly related to location of
ischemia
Intermittent short episodes of
impaired function
* e.g., muscle weakness in
arm or leg
Visual disturbances
Numbness and paresthesia
Transient aphasia or confusion
may develop.
Transient
Ischemic
Attacks Diagnosis & Management
Diagnosis
- Important to rule out other
causes
- MRI (preferred), CT scan
- Carotid doppler
- Angiography
Management
- Risk stratification
- Initiation of stroke prevention
therapy
Cerebrovascular
Accidents (CVAs)
A CVA (stroke) is an infarction of brain tissue that results from lack of blood.
Ischemic - Occlusion of a
cerebral blood vessel
Hemorrhagic - Rupture of
cerebral vessel
5 minutes of ischemia
irreversible neuronal damage
Cerebrovascular
Accidents Facts
Leading cause of disability
Fifth leading cause of death in US
Common denominator - associated with hypoperfusion
African-American higher risk
Cerebrovascular
Disorders Hemorrhagic Stroke
Third most common cause
Hypertension is primary cause
Bleeding compressed brain
tissue ischemia, edema,
increased ICP and necrosis
Types
- Intracerebral hemorrhage
- Subarachnoid hemorrhage
Cerebrovascular
Disorders S&S
Depend
- Location of obstruction
- Size of artery involved
Contralateral motor & sensory deficit
Initially flaccid paralysis
then spastic paralysis develops weeks later
NIH Stroke Scale (NIHSS)
- To assist with rapid diagnosis
- Predict size and severity
- Predict short- and long-term
outcomes
Stroke S&S
Abrupt onset of hemiparesis, hemisensory deficits
◦ Monocular or binocular visual loss
◦ Visual field deficits
◦ Diplopia
◦ Nystagmus
◦ Dysarthria
◦ Facial droop
◦ Ataxia
◦ Vertigo (rarely in isolation)
◦ Aphasia
◦ Headaches
◦ Sudden decrease in level of consciousness
Stroke Treatment
Focused on restoration of
perfusion, counteracting ischemia,
and prevent necrosis
Fibrinolytic (tPA) – 4.5 hours or less
Antiplatelet agents (aspirin)
Mechanical thrombectomy
Blood pressure control
Glucocorticoids
Supportive treatment
Occupational, physical, speech,
rehabilitation begins immediately.
Treat underlying problem to prevent recurrences.
Stroke Prevention
Cardiovascular disease: platelet
antiaggregant aspirin
Hyperlipidemia - statins (cholesterol
lowering drugs)
Healthier diet
Control hypertension – antihypertensive
Control diabetes type II
STOP smoking
Exercise to decrease weight
Lifestyle modifications/interventions
Infection and Inflammation of the CNS
Meningitis
- Bacterial
- Viral (aseptic)
- Fungal
Meningitis Pathophysiology
◦Routes of Inoculation
◦ Hematogenous
◦ Direct contiguous spread
◦Organisms
◦ Neisseria meningiditis
◦ Streptococcus pneumonia
Meningitis Treatment
- Rapid diagnosis and
treatment essential to
prevent morbidity and
mortality
◦ Aggressive
antimicrobial therapy
◦ Glucocorticoids
◦ Reduction of cerebral
inflammation and edema
◦ Vaccines are available
Multiple Sclerosis
◦ Autoimmune
◦ Progressive, inflammatory,
demyelinating disease of the central
nervous system
◦ 1 : 100,000 in US and Europe
◦ Women : men – 2 : 1
◦ Age: 20-40 years
◦ Relapses/remissions
◦ In time, neural degeneration becomes
irreversible.
◦ Function is lost permanently
Multiple Sclerosis Pathophysiology
◦ Inflammation: demyelination: axonal degeneration
◦ Target oligodendrocytes
Multiple Sclerosis: S&S
◦ Manifestations determined by areas of demyelination
◦ Paresthesia, areas of numbness, burning, tingling
◦ Weakness
◦ Impaired gait
◦ Visual disturbances
◦ Blurred vision
◦ Diplopia (double vision), scotoma (spot in visual field)
◦ Urinary incontinence
◦ Loss of coordination, bladder, bowel and sexual dysfunction
◦ Dysarthria - weakness in the muscles used for speech
Multiple Sclerosis Diagnostics
Complete neurological examination
No specific marker
MRI for diagnosis and monitoring –
test of choice
Cerebrospinal fluid analyses
Evoked potential tests
Multiple Sclerosis Treatment
No definitive treatment approved at this time
Several research trials in progress
Therapy includes physical therapy, occupational therapy
Manifestations require individual attention.
