Final Flashcards
Herpes Simplex and Varicella remain dormant
In sensory ganglia
Post Herpetic Neuralgia
Severe pain along nerve pathway
Condition seen especially in people >60 y/o
Rarely is also motor paralysis
PT role in management of person with varicella zoster
Keep track of strength
Possibly manage pain
Stages of HIV infection
Early stage (Asymptomatic): CD4 count >500. No need for retroviral txt Middle stage (symptomatic): CD4 count 200-500. Retroviral probably needed Late stage (advanced disease): CD4 count
Goal of txt of HIV
Minimize viral load
More load = more rapid disease progression
Viral load is prognostic indicator
Opportunistic infections for HIV pt
ADC = HIV Encephalopathy or Dementia Complex
Cryptococcal Meningitis
Viral Encephalitis
Progressive multi focal leukoencephalopathy
Toxoplasmosis
Herpes
Cytalomegavirus
AIDS Dementia Complex
The most common neurological complication of AIDS; major cause of dementia in the young
“HIV encephalopathy”
1/4 ppl with HIV
Symptoms of ADC
Apathy Social withdrawal Difficulty concentrating Difficulty with complex mental tasks May be mistaken for depression
All changes in affect
Patient with HIV walks into your clinic. The patient exhibits these behaviors upon your examination that make you think ADC
Slowing of verbal and motor tasks
Unsteady gait
Decreased ability to perform repetitive movements (not dysdiakinesia)
Needs txt because pt will eventually be mute, bedridden, paraplegic, and incontinent.
What is the link between Cerebral Toxoplasmosis and HIV patients?
CATS!
Patients should be using gloves and masks when cleaning litterbox
Inflammatory Demyelinating Polyneuropathy (IDP)
Asymptomatic patients present with weakness but without sensory loss
Primary CNS tumors
Develop/start in the brain, SC or supporting tissues
Do not typically metastasize from the brain to other parts of the body due to the lack of a Lymphatic system in the brain
Metastatic Tumors
Travel to the CNS from other sites (lungs, breast, GI tract, GU tract, Melanomas)
Can spread from one part of the CNS to another via the CSF
Effects of a Space Occupying Lesion
Mechanical displacement of brain and SC. Will damage and destroy brain tissue
Blockage of CSF circulation. In young -> hydrocephalus. In adult -> increased ICP
What is a focal neurological deficit?
A problem in nerve, spinal cord, or brain function that affects a specific location. Ie: left arm, right arm
Also refers to any problem with a specific nervous system function
Clinical signs of Elevated ICP
Headache
Seizures
Headache associated with increased ICP
Worse with straining activities (coughing, lifting, etc)
Awakens person from sleep
Worse in AM; may get better during the day d/t erect position causing drainage
Often accompanied by nausea, vomiting and papilledema
Seizures are more likely to accompany
Slow growing tumors
Differentiation
The extent to which parenchyma like cells resemble their normal forbearers morphologically and functionally
The more differentiated the cell, the more similar it is to its original cell type, both morphologically and functionally. Is better than poorly differentiated
Anaplasia
Hallmark of malignancy
When malignant cells are composed of undifferentiated cells; Do not have specialized functional activity
The less differentiated the cell
The less similar it is to its original cell type, both morphologically and functionally
The tumor cell cannot perform the originally intended/needed functions
“Cells are well differentiated” is this good or bad? What does it mean?
It’s good bc cells are able to do their specialized function
“Cells have high degree of Anaplasia” is this good or bad? What does it mean?
It’s bad. Means they’re malignant, undifferentiated. Have no specialized function
“Cells in sample are undifferentiated” is this good or bad? What does this mean?
Bad. Cells are different from what they were originally
Tumor grading
G1: well-differentiated (low grade)
G2: moderately differentiated (intermediate grade)
G3: poorly differentiated (high grade)
G4: undifferentiated (high grade)
TMN staging system
T - tumor size
M - metastasis
N - nodes
I-IV staging system of CNS tumors
I - no spread beyond structure of origin
II - spread into adjacent tissue
III - spread beyond own region, but not distant
IV - involves another organ or distant site
Neurinomas
Slow growing benign tumors that originate from Schwann cells
Typically develop in vestibular portion
Clinical presentation is sensorineural hearing loss, tinnitus, and vertigo
CD4 Count
Normal T cell count = 500-1500
LMN lesion signs
Hyporeflexia or Areflexia Hypotonia Fasciculations and Fibrillations Muscle weakness Atrophy
LSN lesion signs
Hyporeflexia/Areflexia
Dermatomal pattern of paraesthesia/anesthesia, hypoesthesia, hyperesthesia
Neuropathy
Disorder of the nerve
Myelinopathy
Disorder of the myelin; due to disease state
Dying Back Neuropathy
Progression of disease state and signs/symptoms distally to proximally. Starts at the most distal parts of the nerve fiber and progresses proximally approaching the cell body.
Guillan-Barre Syndrome (GBS)
Acute Inflammatory Demyelinating Polyneuropathy (AIDP)
Most common in 5th-8th decades of life. Females > Males. White > Black
Is idiopathic
Possible autoimmune response that damages peripheral nerves
Risk Factors linked to Guillan-Barre Syndrome
Most cases are preceeded by cases of:
Infections: Bacterial (Campylobacter jejuni)
Viral (Haemophilus influenza), Epstein-Barr, CMV
Surgery
Vaccination (H1N1)
Pathogenesis of Guillan-Barre Syndrome (GBS)
Believed to be autoimmune attack on PNS myelin
Affects PNS from spinal nerve roots to distal termination of motor and sensory fibers
Inflammatory response results in macrophages and lymphocytes that strip myelin from PNS nerves
*Affects nerve roots and peripheral nerves
*Damages myelin sheath
Remyelination
Mediated by Schwann cells
Recovery results in shorter internodal distances
Clinical Presentation of GBS
Rapidly evolving
Ascending symmetrical motor and sensory deficits with sparing of extraocular muscles
Usual progression of bilateral paralysis/paresis is from distal to proximal
Weakness may be only in extremities or may result in tetraplegia along w/ involvement of respiratory muscles and cranial nerves. Dysphagia often present
Areflexia
Paraesthesias and hypersthesias. Pain often present. “Stocking-glove presentation”
Some ANS involvement: Decreased cardiac output, tachycardia, BP fluctuations, cardiac rhythm changes, possible sudden death
Most common cause of mortality in GBS
Respiratory failure, so mechanical ventilation required ~30% of patients
Recovery from GBS
Can last months to years, occurs in a proximal to distal manner
GBS Phases
Actue phase (Onset to about 2-4 weeks) Static phase (weeks 3-5, about a 4 week period w/ stable conditions but sxs still present) Gradual Recovery (months to years)
Medical Management of GBS
Plasmapheresis
High does IV administration of immunoglobulin
Interventions for Management of GBS
Pulmonary PT Position and ROM Motor Learning Strengthening Functional Training Education
More is better w/ a GBS patient RIGHT?! No Pain no gain
No it’s a possible contraindication to exercise
Avoid muscle fatigue; it can lead to significant loss of strength
Provide freq rest periods
Only GENTLE stretches
Return to bedrest if decrease in function or strength occurs
Overwork of respiratory muscles may lead to profound decrease in respiratory function
Acute Poliomyelitis
Viral in origin
Affects the anterior horn cell
Presentation is asymmetrical: Effects proximal > distal; including trunk. LE > UE
SxS of Acute Poliomyelitis
1st 2 weeks: fever, malaise, myalgia, sore throat, GI upset
Flaccid paralysis
Hyporeflexia or areflexia
Sensation intact. Myalgia can be intense
Bulbar symptoms: Dysarthria, Dysphagia, Extraocular sparing, Death d/t respiratory involvement
Recovery from Acute Poliomyelitis
Restoration of neurons not irreversibly damaged. Collateral sprouting from surviving axons
Compensation via hypertrophy of undamaged muscles = “denervation hypertrophy”
Many individuals use muscle substitution to achieve functional goals
Often ligaments are used for stability -> ligamentous hypermobility and eventually malalignment of trunk and limbs
Polio is long gone right?
NOO!