Neuro Pathology Flashcards
Alzheimer’s Disease Brain involvement
- Cerebral Cortex and Subcortical areas
- Deterioration of neurons involved with ach transmission -Formation of amyeloid plaques and neurofibrillary tangles => further deterioration
AD Etiology
- No exact known cause
- Risk increases with inc age
- Higher incidence in women
AD Treatment
-Meds to inhibit acetylcholinesterase, alleviate cognitive symptoms and behavioral changes
Common meds for AD
- Tacrine (cognex): cholinergic agent
- Donepezil (aricept): cholinergic agent
- Rivastigmine (exelon)
PT management with AD
- Focus on maximizing pt’s remaining function
- Family/caregiver education
Progression of AD (3)
1) Initial: change in higher cortical functions (learning new things, memory/concentration)
2) Progression: loss of orientation, rigidity, bradykinesia, shuffling gait, impaired ability to perform self-care
3) End-stage: severe intellectual/physical destruction, incontinence, functional dependence, inability to speed
Amyotrophic Lateral Sclerosis (ALS) Presentation
- Presents with both upper (d/t demyelination of corticospinal and corticobulbar tracts) and LMN (d/t anterior horn cell loss in the SC and motor cranial nerve nuclei in lower brainstem) impairments
- Rapid degeneration => dennervation of muscle fibers, muscle atrophy, weakness
Amyotrophic Lateral Sclerosis (ALS) Etiology
- unknown exact cause
- higher incidence in men
- commonly begins at 40-70 years of age
Amyotrophic Lateral Sclerosis (ALS) signs and symptoms (UMN vs LMN s/sx)
- UMN: incoordination, spasticity, clonus, positive Babinksi
- LMN: Asymmetric* muscle weakness, fasiculations, cramping, atrophy within the hands.
- Will exhibit fatigue, oral motor impairment, motor paralysis, and eventual respiratory paralysis
Common meds for Amyotrophic Lateral Sclerosis (ALS) (1)
-Riluzole (Rilutek)
PT intervention for ALS
- Focus on quality of life
- Family/caregiver treatment
Bell’s Palsy Presentation
- assymetrical facial involvement
- Eyelid and mouth drooping
- Drooling
- Dry eye
- Inability to close eye d/t weakness
What nerve is affected with Bell’s Palsy?
-Facial Nerve
Bell’s Palsy Etiology
- Herpes simplex/zoster virus thought to be a cause
- Inflammation within auditory canal injures nerve and => demyelination of the nerve (axonal degeneration if apoxia occurs)
Common (types) of meds for Bell’s Palsy (2)
- Anti-viral meds
- Corticosteroids
PT for Bell’s Palsy
- Less severe cases resolve within 2 weeks with no intervention
- Stimulation of facial nerve
- Facial massage/exercise
Carpal Tunnel Syndrome (CTS) signs/symptoms
- Motor and sensory disturbances in median nerve distribution d/t Median Nerve entrapment
- Paresthesias may radiate into the UE, shoulder, and neck
- Night pain
- hand weakness
- muscle atrophy
- decreased grip strength/clumsiness
- decreased wrist mobility
CTS treatement
- splinting
- ergonomic changes
- local corticosteroid injections
- PT
- Carpel Tunnel release (severe cases)
Types of Cerebellar Disorders (4)
1) Congenital Malformations
2) Hereditary ataxias
3) Spinocerebellar ataxias
4) Acquired ataxias
Congenital Malformation
- Type of Cerebellar disorder
- Manifest early in life, non-progressive
- Ataxia usually present
Spinocerebellar Ataxia
- Type of Cerebellar Disorder
- main autosomal dominant ataxia
- affect multiple areas of the CNS and PNS
- neuropathy, pyramidal signs, ataxia, and restless leg syndrome
Acquired Ataxias
- Type of Cerebellar Disorder
- Nondenerative systemic disorder, toxin exposure, or idiopathic in nature
- i.e. alcoholism, hypothyroidism, and vitE deficiency
Hereditary Ataxias
- autosomal dominant
- Autosomal recessive = Fredrich’s ataxa (gait unsteadiness, upper extremity ataxia, dysarthria, paresis, declined mental function).
Cerebellar Disorders s/sx
- depends on affected areas
- ataxia
Diabetic Neuropathy Nerve Damage
-Microvascular diases combined with effects on nerves from hyperglycemia => nerve ischemia
Diabetic Neuropathy s/sx
- Symmetrical pattern of weakness and sensory distrubances (“stocking-glove” distribution)
- May involve sensory, motor, or autonomic systems
Diabetic Neuropathy Treatment
- Monitor blood glucose levels
- PT for pain management, foot care, overall fitness
Epilepsy
- Chronic condition where temporary brain dysfunction => seizure
- Unprovoked and unpredictable
Epilepsy etiology
-many cases idiopathic
Conditions leading to increased risk of Epilepsy (7)
- genetics
- head injury
- dementia
- CVA
- Cerebral Palsy
- Down Syndrome
- Autism
Epilespy Treatment
- Antiepileptic meds (major side effects)
- Possible surgical intervention
Guillain-Barre Syndrome (GBS) aka Acute Polyneuropathy
- temporary inflammation and demyelination of peripheral nerves due to attack from GBS autoantibodies
- Peak in frequency in young adults and between 5th-8th decades
Etiology of GBS
-hypothesized autoimmune response to a previous respiratory infection, influenza, immunization, or surgery
GBS s/sx
- motor weakness in distal-proximal progression
- sensory impairment
- potential respiratory paralysis (life-threatening)
- absence of DTRs
- Inability to speak/swallow
Time to peak level of disability with GBS
2 to 4 weeks after onset
PT treatment with GBS
- pulmonary PT
- strenghening
- mobility raining
- w/c and orthotic prescription
- AD training
Huntington’s Disease (HD) aka Huntington’s Chorea brain involvement
- Degeneration/atrophy of the basal ganglia and cerebral cortex
- Deficient neurotrasmitters => unable to modulate movement
HD etiology
- Autosomal dominant trait linked to chromosome 4
- average age 35-55 years
HD s/sx: inital stage
- involuntary choreic movements
- mild personality changes
- grimacing/tongue protrusion
- ataxia with choreathetoid movements
HD s/sx: late stage
- mental deterioration
- decrease in IQ
- depression
- dysphagia
- incontinence
- immobility/rigidity
PT for HD
-maximize endurance, strength, balance, postural control, and functional mobility
Mutliple Sclerosis (MS) brain involvement
- patches of demyelination in brain and SC
- subsequent plaque formation
- evental failure of impulse transmission
MS etiology
- unknown, but theorized is an autoimmune repsone from a slow-acting virus combined with genetic and environmental factors
- highest incidence 20-35 years old
MS s/sx
- Periods of relapse and remission
- initially visual problems
- parethesias
- clumsiness/weakness
- ataxia
- balance dysfunction
- fatigue
PT for MS
- regulate activity level
- energy conservation techniques
- normalize tone
- balance/gait training
- core stabilization
- adaptive/assistive device training
Myasthenia Gravis
- autoimmune diease
- antibodies block/destroy ach receptors in synapse and prevent muscle contraction => weakness
Myasthenia Gravis etiology
- autoimmne disease associated with an enlarged thymus
- association with other autoimmune disorders
- range from mild-severe involvement
Myasthenia Gravis s/sx
- remissions and exacerbations
- extreme fatiguability
- muscle weakness (occular muscles typically affected first)
- dysphagia, dysarthrira, and cranial nerve weakness
PT for Myasthenia Gravis
- pulmonary intervention
- energy conservation techniques
- isometric strengthening exercises
Parkinson’s Disease
- degenerative disorder d/t decrease in dopamine production within basal ganglia
- 50-79 year olds are majority diagnosed
- PT focuses on strength, endurance, and functional mobility
Post-Polio Syndrome
-Occurs when compensated reinnervation from Polio fails and results in ongoing muscle denervation
PPS s/sx
- Slow and progressive weakness
- fatigue
- muscle atrophy
- pain
- trouble swallowing
PPS treatment
- no deds to alter progression
- lifestyle modification and symptomatic intervention
PT for PPS
- encourage supervised exercise
- functional independence
- adaptive equipment
- education
