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Clinical neuro > Peripheral diseases > Flashcards

Peripheral diseases Flashcards

1
Q

Distal Axonal Degeneration

A

Aka “dying-back neuropathy”

● Neuronal cell bodies and proximal axons intact

● Axon regeneration = nerve function return

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2
Q

Neuronopathy

A

● Little potential for recovery

death of neuronal cell body

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3
Q

Wallerian Degeneration

A

● Axonal degeneration that occurs in a nerve distal to transection or crush

may regnerate if not too proximal

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4
Q

Segmental Demyelination

A

Loss of myelin form 1 or more internodes (dysfunctioned schwann cells)

Primary demyelination
Secondary demyelination

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5
Q

what is remyelination step for segmental demyelination

A

Schwann cells can proliferate → remylinated internodes have shortened internodal length

○ Remyelination of demyelinated segments

○ Recovery of function

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6
Q

Chronic Demyelinating Neuropathies

A

Repeated episodes of segmental demyelination and remyelination of peripheral nerves

Onion bulb = segmental demyelination followed by remyelination of peripheral nerves

○ Leads to hypertrophic neuropathy (enlargement)

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7
Q

Peripheral Neuropathies etiologies

A

DM = most common cause of generalized peripheral neuropathy in US

● Etiology

Alcohol

Drugs

Diabetes
Heavy metal poisoning

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8
Q

Guillain - Barre Syndrome

A

Acquired

○ Campylobacter jejuni

○ Cytomegalovirus

○ Epstein-Barr virus

○ Mycoplasma pneumoniae

● Immune mediated

○ Causes lymphocytes to attack axons

● Acute inflammatory demyelinating polyradiculoneuropathy

● Neuromuscular paralysis

○ Symmetric

○ Begins distally and ascends proximally

● Symptoms

○ Cardiac arrhythmias

○ hyper/hypotension

● CSF

○ High protein

○ Low WBC’s

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9
Q

symptoms of guillain barre syndrome

A

Acquired

○ Campylobacter jejuni

○ Cytomegalovirus

○ Epstein-Barr virus

○ Mycoplasma pneumoniae

● Immune mediated

○ Causes lymphocytes to attack axons

● Acute inflammatory demyelinating polyradiculoneuropathy

● Neuromuscular paralysis

○ Symmetric

○ Begins distally and ascends proximally

ascending paralysis

● Symptoms

○ Cardiac arrhythmias

○ hyper/hypotension

● CSF

○ High protein

○ Low WBC’s

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10
Q

guillain bare syndrome and CSF

A

● CSF

○ High protein

○ Low WBC’s

• Albuminocytologic dissociation

TYPICAL CSF FINDINGS ARE AN ALBUMINOCYTOLOGIC DISSOCIATION WITH INCREASED PROTEIN AND FEWER THAN 5–10 WBCS

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11
Q

Charcot Marie Tooth Disease - CMT

A

● Chronic inflammatory demyelinating polyneuropathy

axonal demeylination

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12
Q

different types of CMT

A

CMT1 = most common
○ Multiple genes/loci (PMP22) that lead to this

■ Messed up chromosome 17

● CMT2 = less common

● CMTX
○ X-linked (CMTX)

○ Aka CMT 4 (autosomal recessive)

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13
Q

what gene is mutated in charcot marie tooth disease

A

PMP22

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14
Q

symptoms of charcot marie tooth disease

A

Symptoms

○ Muscle dystrophy - high arch, clawing of toes

■ Distal muscle wasting

○ Deep tendon reflexes = gone

○ Steppage gait = foot drop

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15
Q

Dejerine - Sottas Syndrome

A

AKA “CMT3”, but resembles CMT1

● More severe

○ Onion bulbs

○ Axonal loss

● Early infancy

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16
Q

Amyotrophic Lateral Sclerosis (Ice bucket challenge)

A

Lou Gehrig disease

● Onset = 55

● Men > women

● Die within 3 years

● “Seek care when weakness begins to affect activities of daily living”

● Exclusive motor involvement and the chronologic course distinguish it

● Painless with discomfort with loss of normal abilities

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17
Q

Amyotrophic Lateral Sclerosis (Ice bucket challenge) symptoms

A

Progressive weakness and atrophy

○ Dragging gait - foot drop

○ Fine movements lost in hands

○ CN involvement = LMN in ALS

■ Example = deviated tongue; hypoglossal CN 12

○ Weak neck extension/flexion

○ Ventilation problems near end of life

■ Abdomen moves out instead of in during breathing

18
Q

Mild Cognitive Impairment

A

Longitudinal follow-up of these patients reveals a substantially increased risk of

cognitive decline and eventual “conversion” to dementia

19
Q

Alzheimer disease

A

Confused

● Short-term memory loss, cant recall details

● “Overblown concerns”

● Forgets things easily

Gave up old activities

● MRI = atrophy

● Strokes

● Diabetic more likely to develop

○ Hemoglobin A1C elevated

● Dementia - most commonly caused by AD

● High risk of AD in down syndrome patients

● Older > younger

● MMSE low score

○ Tests cognitive function

20
Q

what causes alzheimers disease

A

Beta-amyloid protein build up in brain (from APP - amyloid precursor protein)

○ Alpha-beta peptides form pathogenic aggregates = plaques ■ Tangling of plaques causes AD

21
Q

● Neurofibrillary tangles

A

Pathologic hallmark of AD

○ Number and tangles = direct severity of dementia

○ Made up of microtubule-associated protein tau

Helical shape

Neuronal cytoskeleton structure

○ Found during autopsy

22
Q

what differentiates AD from other dementias

A

● ABSENCE of motor deficits early in AD differentiates it from most other dementias

23
Q

what is MALCOPE (AD)

A

MALCOPE = Memory, Attention, Language, Construction, Orientation, Praxis (skills),

and Executive function

24
Q

alzheimers and CSF

A

○ Decreased B amyloid / increased tau/phosphotau protein

25
Q

what is not a diagnositic of AD

A

● ApoE genotype IS NOT diagnostic of AD

26
Q

Lewey Bodies

A

Confusion

● Depression

● Hallucinations

● Forgetful

● Parkinsons as a prior diagnosis

○ Hallmark is LB presence

● Diagnosis

○ Presence of LB pathology regardless of AD pathology

27
Q

Frontotemporal Lobar Dementia

A

related to a degenerative process primarily confined to the frontal and temporal lobes

Change of personality

● Forgetful

● Developed OCD

● Hard to remember names

● Lateral frontal lobe atrophy

○ Or temporal lobes

● Intellectual decline

● AKA Pick disease

● Most ages it can start

● Hereditary

28
Q

symptoms of frontotemporal lobar dementia

A

Symptoms

○ Low hygiene

○ Social behavior decline

29
Q

behavior subtypes of frontotemporal lobar dementia

A

3 major behavior subtypes

○ Disinhibition

○ Apathy

○ Stereotypic behavior

30
Q

proteins associated with frontotemporal lobar dementia

A

TDP43

31
Q

Vascular Cognitive Impairment

A

Inactive

● Low motivation

● Gave up previous interests

● Feels off balance when making turns

○ Bad gait

Hypertension, cardiovascular disease (at risk for stroke)

○ Not taking medication

● Not happy

● Bilateral babinksi sign

● Cant think for him/herself

32
Q

● Most common cause of Acute spinal cord syndrome

A

metastatic deposits

33
Q

what are metastatic deposits

A

Most common cause of Acute spinal cord syndrome

● Old people

● Spinal metastatic lesion

○ Usually presents as a tumor elsewhere before

● Leg weakness

○ Impaired gait

● Urinary retention

34
Q

Infarctions

A

Occlusion of anterior spinal artery

● Aortic dissection

● Embolism

● Hypotension

● Paraparesis

○ Sensory loss
● Poop themselves - sphincter control lost

35
Q

Distractive Flexion

A

Severe flexion of neck with rotation

● Most common

● Posterior ligaments injured initially

○ Spinous processes distance increases

● Examples: car accident or fall

36
Q

most common type of spinal trauma

A

distractive flexion

37
Q

Compressive Flexion

A

Axial loading with acute severe flexion of the neck

● Example: Diving into shallow water, thrown out of vehicle

● Burst vertebral body

● Commonly C4-5 & C5-6

38
Q

Distractive Extension

A

Hyperextension of the spine

● Whiplash !

○ Most minor form
● Elderly patient falling with cervical spondylosis or stenosis

○ Hit forehead
● No traumatic radiographic abnormality

● SC pinched between anterior ostephytes and in-buckled ligamentum flavum

39
Q

Compressive Extension

A

Axial loading with hyperextension

“teardrop fracture”

● Laminar frx = minor

● Teardrop frx = major

○ Anterior longitudinal ligament

○ Avulsion frx - pedicles/lamina messed up

40
Q

Cervical spine injury: Hospital setting

A

USUALLY after initial traumatic injury

○ From transport and st00f

● Altered mental status have a risk factor

● 15% of injuries are multiple

● Use cervical collar

41
Q

how to diagnose peripheral neuropathies

A

Many neuropathies do not show additional disease-specific histologies beyond axonal loss or demyelination, so clinicopathologic correlation is necessary to establish cause

42
Q

what are lewy bodies

A

• They are the hallmark histopathologic lesions of primary PD where these occur within neurons of the substantia nigra and other brainstem nuclei

Clinical neuro (3 decks)

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