patho final (copy)

(SP)

right vs left hemisphere cva

right hemisphere: you become a hot headed asshole

left hemisphere: kinda slow but methodical and logic remains intact

cva prognosis

1/3 die within first 3 weeks

highest risk of mortality = initially comatose
next highest risk of mortality = hemorrhagic

30-40% severe disability

30% require assistance with ADL, 60% eventually home bound

amyotrophic lateral sclerosis (ALS)

progressive motor neuron disease

idiopathic

leads to degeneration and scarring of motor neurons in lateral spinal cord, brain stem, cerebral cortex

ALS incidence (M or F)?

age of onset?

familial factors?

M > F

mid 50s

chromosome 21 (inherited autosomal trait) or chromosome 2 (recessive gene)

ALS pathogenesis

degeneration and loss of motor cells

• spinal cord: spinocerebellar tracts, anterior horn cells, brainstem

diffuse loss of myelin in all areas except posterior column

ALS UMN vs LMN lesion pathogenesis

UMN: giant pyramidal cells, neurons, and dendrites affected
corticospinal and corticobulbar tracts abnormal

LMN: anterior horn cells damaged in spinal cord and brain stem

UMN vs LMN lesion clinical manifestations

LMN: (LOW = weakness, atrophy, etc)
- cell death and early denervation
- insidious development of asymmetrical weakness (distal aspect of 1 limb)
- cramping
-weakness + atrophy of msucles
- fasciculations (involuntary muscle vacillations)
- extensors weaker than flexors

UMN: (uppers make you hyperactive)
- positive babinski/hoffman’s
disproportionately active reflexes (3+, 4+)

what would you expect to see with ALS?

50% have cognitive impairment (visual attention, working memory, problem solving, verbal fluency, dysarthria)

eye movement, sensory, bowel+bladder function preserved

ALS diagnosis

physical exam

EMG (presence of fibrillations and fasciculations)

muscle biopsy (denervation and atrophy)

muscle enzymes (elevated creatine phosphokinase)

what are pharmacological treatments of ALS?

baclofen/diazepam for treatment of spasticity

ALS prognosis

earlier dx, longer the course

adult onset death in 2-5 years (primarily from pneumonia)

later stages can have respiratory failure and inability to eat

alzheimer’s vs dementia

AD: progressive disease that attacks brain and results in: impaired memory, thinking, behavior interfering with daily function until death

dementia: decline in intellectual functioning severe enough to interfere with person’s relationships and ability to carry out ADLs

dementia is a decline in intellectual functioning while AD is a progressive neurodegenerative disorder

what kinds of dementia are irreversible?

degenerative diseases: PD, MS

infections: neurosyphilis, AIDs

vascular disease: CVA, anoxia

alzheimer’s incidence (M or F)

age?

F 2.8x > M

early = <65
late = > 65

primary risk factors of ALS

age
family hx
genetic markers
trisomy 21
F
CV risk factors

possible protective factors

ApoE2 allele
fish consumption (omega 3s good for brain function)
higher education
regular exercise
moderate EtOH intake (alcohol)

AD pathogenesis

failure to sustain brain cells (neuronal death, loss of synaptic connections)

progressive accumulation of insoluble amyloid (plaques)

plaques trigger inflammatory response

ACh depletion correlates with severity of AD

huntington’s disease

progressive hereditary neurodegenerative disorder characterized by abnormalities of movement, personality, disturbances, and dementia

choreic movement: involuntary spasmodic twitching/jerking in muscle groups not associated with production of purposeful movements

at what age does huntingdons usually begin

middle age (25% post 50yo)

huntington’s pathogenesis

atrophy of basal ganglia (caudate nucleus and putamen)

huntington’s movement disorders

abnormal restlessness involving UE and face
chorea increased by emotional stimuli, complex motor tasks, concentration
abnormal rigidity
occular movement defects
dysarthria/dysphagia
cachexia

huntington’s psychiatric disorders

personality and behavior changes (irritability, apathy, depression, violence, emotional lability)

memory disturbance

visuospatial deficits

affective disorder

huntington’s prognosis

death 15-20y post diagnosis

survival into 80s uncommon

suicide

MS

most common demyelinating disease of CNS

sclerotic plaques block nerve transmission (found throughout CNS)

autoimmune

4 types of MS

relapsing-remitting: most common (85% of newly dx)

secondary progressive: 60% will progress to this within 20 y onset

primary progressive

progressive relapsing: rarest

MS incidence (M vs F)

age

F 2.5 > M

incidence rises steadily from teen - 35

optic neuritis is a sign of?

MS

unilateral loss of vision, p!

trigeminal neuralgia and lhermitte’s sign are significant for?

MS

trigeminal neuralgia: damage to trigeminal nerve causing electric shock pain

lhermitte’s: neck flexion causing quick electric shock

what motor impairments would someone with MS have

dysmetria, dyssynergia, dysdiadochokinesia, postural tremor, vertigo, dysarthria, dysphagia

MS diagnosis

MRI critical (evidence of lesion and attack)

MS prognosis

no cure

suicide rate > 7x

W better prognosis > M

parkinson’s

chronic progressive disease of motor component of CNS characterized by:

rigidity
tremor
bradykinesia
postural instability

parkinson’s prevalence (race)

age

white > black

inc age = inc incidence

parkinsons risk factors

lower risk with smoking, exercise

inc risk with toxic/infection exposure, higher education

parkinson’s pathogenesis

basal ganglia dysfunction (area responsible for premotor initiation and scaling, SN degen)

→ decreased dopamine production (70-80% prior to clinical signs)

hallmark signs of parkinson’s

bradykinesia
akinesia
muscular rigidity (cogwheel, lead pipe)
resting tremor (pill rolling)
masked face

postural deficits (neck flexion, trunk, hips, knees, kyphosis, scoliosis)

speech (monotone, stuttering, rapid, low pitched, dysphasia, trouble chewing)

bowel/bladder issues

insomnia

parkinson’s triad

tremor, rigidity, akinesia

SCI incidence (M vs F)

age

80% M

mostly early 40s

SCI pathogenesis (primary vs secondary)

primary: necrotic death of axons
spinal shock: period of loss of all reflexes and sensation with flaccidity below level of lesion

secondary: ischemic, necrotic (macrophages), axonal edema and increased vascular permeability, synaptic dysfunction (demyelination)

syringmyelia

clinical condition from collapse of spinal cord after cyst (syrinx) formation

phantom limb

SCI lesion levels

complete lesion: no sensory or motor below level of lesion

incomplete lesion: preservation of some sensory/motor below level of lesion

SCI clinical manifestations

tone:
flaccidity (initially)
spasticity (gradually)

impaired temp control (no sweating below lesion)

skeletal changes (osteoporosis, heterotrophic ossification (bone dev in muscle), scoliosis)

SCI and bladder/bowl/sexual dysfunction

lesions ABOVE conus medullaris: spastic or reflex automatic bladder
lesions @ cauda equina or conus medullaris: flaccid or non-reflex autonomous bladder

can have issues with getting erect, have orgasm, or fertility

what happens with injuries above t6

htn
bradycardia
HA
profuse sweating above lesion
restlessness
goosebumps
blurred vision

autonomic dysreflexia

TBI incidence (age)

M or F

early childhood (0-4), late adolescence/early adulthood (15-24), elderly > 75yo

M 2x > F

TBI clinical manifestations

motor: increased tone (spasticity)
posturing: decorticate (UE flex, LE ext) arms in prayer while supine
decerebrate (UE and LE extension) arms straight by side while supine

What group of patients who have had CVA have the highest risk of mortality?

hemorrhagic CVA
ischemic CVA
spinal cord CVA
anterior cerebral CVA

hemorrhagic

Which of the following are the classifications of a traumatic brain injury (TBI)?

primary, secondary, closed, open
subdural, subarachnoid, R, L
UMN, LMN complete and incomplete
tetraplegia, paraplegia, diffuse and GSW

primary, secondary, closed, open

What are the modifiable risk factors associated with CVA?

Age, Alcohol Intake and Type II Diabetes
Smoking, Hypertension (HTN), and Gender
Hypertension (HTN), Obesity and Smoking
Genetics, Cardiac Disease and Oral Contraceptives

HTN, obesity, smoking

A 55 y/o man has been diagnosed with a progressive neurologic disease that affects the corticospinal tracts and the anterior horn cells. He has significant, global weakness in both lower extremities, most notably his quadriceps and gluteals; visible muscle fasciculations and atrophy in his hands; a positive Babinski and Hoffman signs; and difficulty with chewing and swallowing. Sensation is normal. Which of the following is the most likely cause of this constellation of symptoms?

ALS
TIA
MS
PD

ALS

are pressure sores a complication of SCI

yes

A therapist is working on bed mobility with a 28 y.o. male patient with a C5 complete spinal cord lesion. The patient begins to sweat profusely and complains of intense headache and blurred vision. His pulse is weak and slow. Which of the following is the most likely cause of this response?

Autonomic Dysreflexia
Anterior Cord Syndrome
Transient Ischemic Attack (TIA)
Nothing, this is a typical exercise response

autonomic dysreflexia

how do you recognize the signs of stroke?

Face, Arms, Speech, Time
Forehead, Age, Speech, Test
Face, Age, Slurred, Test
Face, Arms, Slurred, Tickle

face, arms, speech, time

sudden, severe HA is a sign of ischemic stroke

false

are women more likely to suffer SCI than men?

no

Multiple plaques of demyelination visible by CT scanning are typical of:

Huntington's Disease
Parkinson's Disease
Multiple Sclerosis

MS