Neuro: ALS, GBS, TIA, CVA, infectious disease Flashcards
Transient ischemic attack
Acute, focal cerebral insufficiency last < 24 hrs
Usually < 60 min.
No residual effects
TIA’s happen more often to males or females?
males
patients who have a TIA have an increased risk for stroke how long after?
highest risk of stroke within 1 month of TIA
TIA presentation
varies patient to patient but recurrent TIA’s usually similar.
symptoms are associated with location of defect.
follow a vascular line
carotid area vs. vertebrobasilar area
onset of TIA’s
onset & recovery abrupt
TIA: carotid area presentation
Weakness, heaviness in contralateral arm, leg or face
Numbness
Dysphagia
Ipsilateral monocular visual loss
TIA: vertebrobasilar area presentation
Dim or blurry vision
Vertigo
Dysphasia
Ataxia
Motor or sensory changes: Ipsilateral face, Contralateral body.
what does ipsilateral mean?
stays on the same side
what does contralateral mean?
crosses over the midline, opposite side of the body.
dysphagia
difficulty swallowing
dysphasia
impairment of speech
TIA: diagnostic
History and physical: Identify any pattern, history, Any vascular problems.
CT, MRI or MRA: Rule out hemorrhage, lacunar infarcts or aneurysms
Carotid doppler studies: Carotid stenosis
Echocardiogram: Assess for cardiac source
lacunar infarcts
tiny infarcts that don’t present with symptoms but can be soon scan
TIA: treatment
Depends upon etiology
Anticoagulation: ASA- No benefit of high dose (up to 1500 mg/day) over lower dose (75-325 mg/day); clopidogrel (Plavix)- Antiplatelet drug; Heparin and warfarin if cardiac related.
Carotid endarterectomy with > 70% stenosis
ALS: definition
A rare, progressive neuro disorder characterized by the loss of motor neurons; Upper and lower motor neurons
ALS: etiology
unknown
ALS: RF
Age: 40-70; Gender: Male; Genetics (10%); Smoking
ALS: prognosis
Death usually occurs around 3 years after diagnosis
ALS: patho
Motor neurons in the brainstem and spinal cord gradually degenerate
Electrical and chemical messages from the brain do not reach the muscles
ALS: CM
Weakness of upper extremities (sometimes begins in the legs), Muscle wasting, Spasticity
Dysarthria, dysphagia, drooling
Cognitive and behavioral changes
Constipation
Sleep problems
Breathing
Discuss the excitotoxicity hypothesis of ALS development and the role of glutamate
Excessive levels of glutamate initiate a cascade of events that lead to neuron death
Glutamate = excitatory neurotransmitter
Why do we think this plays a role? Elevated glutamate levels in the CSF, Antiglutaminergic drug (Riluzole) improves survival.
Riluzole (Rilutek)
Classification: Glutamate inhibitor
MOA: Glutamate antagonist; Reduces damage to motor neurons
Indication: ALS
SE: dizziness, GI upset, hepatotoxicity
Effect on life expectancy? Increases life expectancy & slows down deterioration.
GBS: definition
Autoimmune disorder, Myelin sheath is damaged by autoantibodies
GBS: etiology
Viral infection
Bacterial infection: Campylobacter jejuni
Post Surgery (5-10%)
GBS: onset
days to weeks following a viral infection
GBS: CM
Initially: Weakness/tingling in lower extremities
Ascend to descend pattern
Severity of symptoms increases over hours or weeks
Potentially life-threatening if respiratory muscles are involved
Uncoordinated movements
Numbness and decreased sensation
Loss of bowel/bladder control
Blurred vision- can be an early sign.
Difficulty, breathing, swallowing, chewing
GBS: prognosis
95% survive
75% completely recover
25-30% have residual weakness after 3 years
About 3% may suffer relapse of muscle weakness & tingling many years post initial attack
is there a cure for GBS?
no
Describe the basic drug therapies of GBS
Steroid therapy
High-dose immunoglobulin therapy (IV): Shortens severity & duration, Shortens length of stay
GBS: goal of treatment
Reduce severity and accelerate recovery
meningitis: definition
Acute inflammation of the meningeal tissues of the brain and spinal cord
meningitis: Etiology
Infection (lungs or bloodstream) or penetrating wounds
meningitis: main culprits
Streptococcus pneumoniae and Neisseria meningitidis (bacterial), Enteroviruses (viral)
meningitis: where does it occur?
Pia mater, subarachnoid space, ventricular system, CSF
meningitis: when does it occur?
Fall or winter
meningitis: What does it usually follow?
Otitis or sinusitis or those with an immunocompromised state or PNA
meningitis: age
Older adults (>40yrs)
College students
Prisoners
meningitis: patho
Infection of arachnoid mater and CSF
Inflammatory response and pus secretion
Increase in CSF production
Increase in ICP
meningitis: classic triad
fever, headache, stiff neck
meningitis: other CM
Nausea/vomiting
Photophobia
Altered mental status: Drowsiness → Coma, Seizures (30%)
Meningococcus: Skin rash, Petechiae
Positive Kernig sign: Resistance to leg extension
Positive Brudzinski sign: Neck flexion causes hip/knee flexion
Acute Bacterial Meningitis
Most common form
Fatality rate? High, can kill within hours
Long term effects? Hearing loss, seizures, damage to brain
Acute Viral Meningitis
Milder form, often do not see elevated WBS with lumbar puncture when looking at CSF.
Long term effects? None
Bacterial Meningitis: Treatment
Aggressive Antibiotic Therapy: IV, often multiple drugs used, ceftriaxone (Rocephin); Vancomycin, Acyclovir.
Steroid Therapy
Prophylaxis: Vaccines- Available for Meningococcus, pneumococcus, H. influenzae
encephalitis: definiton
acute inflammation of the brain
encephalitis: etiology
viral
West Nile encephalitis (mosquitoes)
Measles, chicken pox, mumps
Herpes simplex virus-1 (HSV)
encephalitis: CM
Signs appear on day 2 or 3 of infection
Range from mild changes in mental status to coma
Other symptoms: Fever, Headache, N/V, Other CNS changes (such as seizures)
encephalitis: pharmocology
Viral infection: Acyclovir (Zovira) is used for HSV infection, Reduces mortality, Does not reduce neurological complications
Seizure disorders: Antiseizure medications.
Brain abscess: definition
accumulation of pus within the brain tissue
Brain abscess: etiology
Local or systemic infection
Most common = from ear, tooth, mastoid, or sinus infection
Brain abscess: major culprits
Streptococci or staphylococcus aureus
Brain abscess: CM
Similar to those of meningitis and encephalitis: Headache, Fever, N/V
Signs of ICP: Drowsiness, confusion, seizures
Focal symptoms may reflect area of abscess: Example: temporal lobe = visual field defects
CVA: major risk factors
Hypertension
Hyperlipidemia: High cholesterol
Tobacco abuse
Diabetes
Race- African Americans
Oral contraceptives
Age*- advances age
Gender- men
Sickle cell anemia
History of TIA
Atrial fibrillation
CVA: CM
Numbness or weakness on one side of body (face, arm, or leg)
Sudden confusion
Trouble speaking
Slurred speech (dysarthria)
Trouble seeing
Ataxia
Severe headache
Which type of ICH would be evident when doing a lumbar puncture?
Subarachnoid hemorrhage
Most sensitive for detecting a subarachnoid hemorrhage 12 hours after onset of symptoms.
Why would a CT scan be a better option for an initial test than an MRI?
A CT scan can show if there is a hemorrhage and drives treatment.
MRI’s take longer than a CT, remember time is tissue.
Alteplase (tPA)
Class: thrombolytic
MOA: Promotes conversion of plasminogen to plasmin.
SE: Increased risk of intracranial bleeding.
Indication: Acute MI, PE, ischemic stroke
Antidote: aminocaproic acid (amicar)- anti-thrombolytic
causes of thrombotic ischemic stroke?
atherosclerosis
hypercoagulable state
causes of embolic ischemic stroke?
Cardiac source
*Mural thrombus
*Atrial fibrillation: Left atrial thrombus, Inability of atria to contract effectively, Blood can become stagnant
*Venous clot if atrial septal defect or patent foramen ovale
*Thrombus of vegetation of valves: Mitral valve vegetation, frequently infectious in nature
Carotid plaque: Carotid bruit
Hemorrhagic stroke
Bleeding within the brain parenchyma
Associated with long standing, severe hypertension
38% mortality: Minutes to hours
Aneurysm: Bulging of blood vessel
Hemorrhagic stroke: presentation
*Age 30 – 60 years
*High morbidity and mortality rates
*Serious disabilities
*“Worst headache of my life”- Hemorrhagic stroke
*Rapid change in level of consciousness (LOC)
*Irritation of the meninges: Nuchal rigidity: Similar to meningitis, Photophobia
Hemorrhagic stroke: prognosis
Based on Age, Location and size, & How rapid the bleed causes brain distortion and shift on scan
Epidural intracranial hemorrhage (ICH).
between skull and dura
Skull fractures
Arterial
Injury is usually less severe
subdural intracranial hemorrhage (ICH).
below the dura
Bridging veins
Brain moves within skull, vessels don’t
Rapid decline – severe injury
Can be slow: 2-10 days later
subarachnoid intracranial hemorrhage (ICH).
Space between outer arachnoid membrane and pia mater
Area filled with cerebral spinal fluid (CSF)
Rupture of: Cerebral aneurysm, Arterio-venous malformation (AVM)
what is the most common aneurysm that can rupture in the brain?
berry aneurysms.
Arterio-venous malformation (AVM)
blood flow is flowing directly from an artery to a vein without slowing down through the capillaries.
the high pressures weaken the vessel walls that may lead to rupture.
penumbra procedure
go in and try to remove the clots
what are the visuals disturbances that can happen as a consequence of a CVA?
contralateral field blindness
homonymous hemianopia
aphasia
some degree of inability to speak or to comprehend
Expressive aphasia
comprehension intact but cannot express
Receptive aphasia
can communicate but cannot comprehend what is being said ”can’t receive”
Dysarthria
imperfect speech sounds
