Neuromuscular and Nervous System Pathology Flashcards
What areas of the brain does Alzheimer’s affect?
cerebral cortex and subcortical areas
What neurons does Alzheimer’s effect? and what else develops?
ones associated with AcH
amyloid plaques
and neurofibrillary tangles show up
Higher incidence of Alzheimer’s in men or women?
women
Initial signs and symptoms of Alzheimer’s?
As it progresses what happens physically?
higher cortical functions like difficulty learning new things and subtle changes in memory and concentration.
rigidity, bradykinesia, shuffling gait
PT treatment of Alzheimer’s?
maximizing patients remaining function and providing family and caregiver education.
ALS involves both…
There is significant loss of …. in the spinal cord and motor cranial nerve nuclei in lower brainstem produces….
Demyelination of corticospinal and corticobulbar tracts produce…
UMN and LMN
anterior horn cell
weakness and muscle atrophy
UMN symptoms
Higher incidence of ALS in men or women?
men
40-70
LMN signs in ALS
asymmetric muscle weakness, fasciculations, cramping and atrophy in the hands. Weakness spreads distal to proximal.
UMN signs for ALS
incoordination of movement, spasticity, clonus and positive Babinski
Bell’s palsy is secondary to trauma and demyelination of…
facial nerve
Is Bell’s palsy common?
And what ages does it show up in?
yes
15-45
What is the associated cause of Bell’s?
herpes viral infection
inflammation of auditory canal produces subsequent demyelination and can lead to ischemia which can degenerate the nerve axonally.
PT for Bell’s
stimulation of facial nerve
facial massage and/or exercise
Carpal tunnel pressure to be considered CTS.
What is normal?
> 30 mmHg
2-10mmHg
Symptoms of CTS
may radiate into UE, shoulder and neck
night pain, weakness of hand, muscle atrophy, decreased grip, clumsiness and decreased wrist mobility.
Types of cerebellar disorders
congenital malformations
hereditary ataxia
spinocerebellar ataxias
acquired ataxias
Hereditary ataxias
most common
recessive
Friedreich’s ataxia
gait unsteadiness begins early in life and followed by UE ataxia, dysarthria and paresis.
Mental function declines and slight tremors may be seen.
Reflexes, vibration, and position senses are impaired.
Spinocerebellar ataxias
dominant
commonly present with neuropathy, pyramidal signs, ataxia, restless leg syndrome
Acquired ataxias
nonhereditary neurodegenerative systemic disorders
toxin exposure or it can be idiopathic.
Alcoholism, hypothyroidism and vitamin E deficiency.
Toxin causes include carbon monoxide, heavy metals and lithium
Diabetic neuropathy most common types
symmetric polyneuropathy and autonomic neuropathy
Diabetic neuropathy symptoms
wasting of muscles in feet or hands
stocking glove sensory distribution
orthostatic hypotension
weakness
urinary impairments
significant pain
Guillain-Barre Syndrome is aka
acute polyneuropathy
GBS is caused by what they think
autoimmune response to previous respiratory infection, flu, immunization or surgery. Viral infections, Epstein-Barr syndrome etc
Seizures a prodromal period is …(things preceding the seizure). But can occur…..and include….
rare
days or hours prior
mood changes, lightheadedness, sleep disturbances, irritability, difficulty concentrating
aura minutes before
An aura is
simple partial seizure
After someone has a seizure how should you lay them?
on their left side until they have fully recovered which is 5-20 min
Signs and symptoms of GBS
distal to proximal progression, sensory impairment and possible respiratory paralysis.
Initially GBS will present with
distal symmetrical motor weakness, mild distal sensory impairments, and transient paresthesias that progress to head
Level of disability with GBS peaks when?
2-4 weeks after onset
How can GBS be life threatening?
respiratory paralysis, absence of DTRs and inability to speak or swallow
PT for GBS?
pulmonary rehab, strengthening, mobility, w/c and orthotic training
Huntington’s is what?
Genetic how?
age it affects?
degeneration and atrophy of basal ganglia and cerebral cortex
autosomal dominant
35-55
MS occurs when?
Initial symptoms of MS
20-35
visual problems, paresthesias and sensory changes, clumsiness, weakness, ataxia, balance dysfunction and fatigue
Myasthenia Gravis is what?
Defect is specifically in the…
autoimmune disease with neuromuscular junction pathology.
transmission of nerve impulses to the muscles at the neuromuscular junction. Antibodies block or destroy receptors needed for AcH uptake and this prevents muscle contraction
What are some potential causes for myasthenia Gravis?
enlarged thymus
diabetes, RA, lupus and other immune disorders
Cardinal signs of Myasthenia Gravis?
extreme fatiguability and skeletal muscle weakness that can fluctuate within minutes or over an extended period. Ocular muscles are affected first and approx half of patients experience ptosis and diplopia. Dysphagia, dysarthria and cranial nerve weakness also are common
Myasthenia Gravis is cyclical?
yes there are periods of remissions and exacerbations
Myasthenia gravis crisis
is a medical emergency where respiratory muscles are affected and ventilator is required.
Parkinson’s affects what part of the brain
substantia nigra of the basal ganglia
Average age of diagnosis with parkinsons
50-79
Myasthenia gravis can fluctuate in severity from…
hour to hour
Myasthenia gravis proximal or distal muscles affected more?
proximal
What do those with myasthenia gravis have difficulty with?
speech, swallowing, and chewing
Involvement of cranial nerves in myasthenia gravis results in…
eyelid weakness, diplopia, ptosis
Remissions with mysathenia gravis are typically not…
complete or permanent
PT for myasthenia gravis
acquire baseline for respiratory and neurological status
monitor respiratory function continually
positioning to prevent aspiration
educate on osteoporosis using corticosteroids
strength for those with mild to moderate symptoms using moderate to max isometrics
What should you avoid for those with myasthenia gravis?
strenuous exercise and stress
excessive hot or cold
Pos-polio is a ….disease. Affects…. after polio.
PPS occurs when compensated reinnervation from polio…
When does PPS show up?
Signs?
Treatment?
LMN
anterior horn cells
fails
25 years after initial recovery
slow and progressive weakness, fatigue, muscle atrophy, pain and swallowing issues.
no pharmacological intervention. Should focus on lifestyle modifications and symptom managment.
Agnosia
inability to interpret info
Agraphesthesia
inability to recognize symbols, letters, or numbers traced on skin
Agraphia
inability to write
Aelxia
inability to read or comprehend written language
Anosognosia
denial or unawareness of ones illness often associated with unilateral neglect
Apraxia
inability to perform purposeful learned movements or activities even though there is no sensory or motor impairment
Constructional apraxia
inability to reproduce geometric figures and designs
Decerebrate rigidity
corticospinal lesion at brainstem that results in extension of trunk and extremities
Decorticate rigidity
corticospinal lesion at diencephalon where trunk and lower extremities are in extension and UE in flexion
Dysprosody
impairment and rhythm of speech
Fluent aphasia
speech is functional but lacks content
Ideational apraxia
inability to formulate an initial motor plan and sequence tasks
Ideomotor apraxia
personal plans a movement or task but cannot volitionally perform it. Automatic movement may occur
Neologism
substitution within a word that is so severe that it makes the word unrecognizable
Non-fluent aphasia
non functional speech
