Neuro Flashcards
How to ID horizontal axis in the CNS
- Hyperreflexia
- Spasticity: VELOCITY-dependant (need to go fast) “catch” with rapid passive extension of joint
- Sensory changes: often harder to localize*
- Weakness
- Upper Extremity
- Greater weakness of extensor muscles
- Flexor posturing, pronator drift - Lower Extremity
- Greater weakness of flexor muscles
- Extensor posturing, circumduction of leg with gait
How to ID horizontal axis in the PNS
- Hypo-reflexia
- Atrophy/Fasciculation
- Sensory changes
- Dermatomal: Radiculopathy
- Sensory nerve distribution: Mononeuropathy
- Glove/Stocking: Polyneuropathy (starts distally and move proximally) - Weakness
- Unilateral: often focal/single muscle group affected
- Bilateral: generally greater either proximally or distally
How to ID vertical axis in the CNS
- Unilateral vs bilateral sx
- Unilateral symptom: - Could be from any level but think cortex/brainstem first.
- Spinal cord less likely due to narrow cross sectional area.
Bilateral symptom:
- NOT caused by a cortical lesion.
- Lesion could be subcortical, brainstem, or spinal cord
- Part of body affected
- ie: face, upper extremity, lower extremity (or a combination).
- The lesion could be anywhere “upstream” from the most proximal affected area.
How to ID vertical axis in the PNS
- Pay attention to reflexes
- Achilles: S1/S2
- Patellar: L3/L4
- Biceps: C5/C6
- Triceps: C7/C8
- Dermatomes!
- Muscle innervations
What is MS
-Episodic demyelinating events of central nervous system (brain +/- spinal cord)- Axonal damage causes persistent symptoms
-Neurodegeneration (cell death) -
Causes brain to atrophy up to 3x faster than normal.
Describe the epidemiology of MS
- F>M
- 15-45
- Latitude: Increasingly common as you travel further away from the Equator
Risk factors for Ms
- Genetics
- Personal Hx of autoimmune conditions
- Vitamin D deficiency
- Viral infections: Epstein-Barr, Varicella, Cytomegalovirus
Describe the subtypes of MS
- Relapse- -Result from acute demyelinating events
- Normally cause new symptoms - Progression –Due to a combination of incomplete healing after relapses and progressive atrophy of brain/cord.
- Most patients eventually develop progressive disease.
Describe the possible presenting sx of MS (differs based on lesion location)
- Parasthesias
- Weakness
- Spasticity
- Ataxia
- Vertigo
- Urinary/Bowel hesitancy or urgency
- Vision changes: diplopia, decreased color saturation, painful eye movement, visual field deficits.
- Other cranial nerve abnormalities
- Severe fatigue
Describe laters sx of MS that appear w/ disease progression
- Gait impairment/ feeling feet are very heavy
- Imbalance
- Cognitive Impairment
- Sleep impairment
- Easy fatigability with physical activity
- Depression
- Sexual dysfunction
Describe the PE Of MS
- Sometimes exam will be normal. Not all symptoms have associated signs on exam.
1. Use “horizontal” and “vertical” axes to help determine location of new lesions and focus imaging. (CNS SX!)
Possible abnormal findings:
- Motor: Weakness in CNS pattern, spasticity
- Reflexes: Hyperreflexia, clonus, up-going Babinski sign
- Cerebellar: tremor, ataxia, nystagmus, dysarthria
- Sensory: impaired vibratory/pain/light touch sensation, allodynia
- Cranial nerves: afferent pupillary defect, impaired EOMs, facial asymmetry, sensory changes
Tx options for MS
- Goes is disease modification and reduce progression NOT Healing
1. Disease modifying therapy
2. Vit. D goal 50-100
3. HD Steroids 3-5 days (acute tx of relapse,– get better faster, not better better!)
*Ongoing research looking at medications to treat progressive disease/atrophy and improve re-myelination following a relapse.
mechanism for MS meds
- Blockade of blood-brain barrier
- Sequestration of lymphocytes in lymph nodes
- Prevention of rapid lymphocyte replication
- Modulation of T-cell subtypes
How do you manage the sx of MS
- Meds- Be careful not to overmedicate. Most medications with CNS targets can cause sedation, cognitive impairment, imbalance, etc.
- PT (ongoing)- compensate better for neuro impairments and reduce deconditioning
- Smoking cessation
- Assistive device for ambulation
*Goal is functional improvement, not symptom resolution.
What is the important “coordination center” for movement
basal ganglia- Cluster of nuclei in the subcortical grey matter
the basal ganglia has connections to:
- cortex
- thalamus
- brainstem
- cerebellum
*All efferent and afferent neurons from you brain come together at the basal ganglia
Smaller and slowness of movement execution, often with reduced movement amplitude
Bradykinesia
*often seen in parkinsons
increased muscle tone in both agonist and antagonist muscles, not velocity-dependent
Rigidity
stiffer- harder to flex, test w/ elbows and ankles
rhythmic muscle contraction/relaxation causing oscillating movement
Tremor
internal restlessness and need to move
Akathisia
irregular, discrete and often sequential* involuntary movement
Chorea
dance like movement
slow, involuntary, writhing movement. A type of slow chorea
Athetosis
patterned, twisting movement caused by intermittent or sustained muscle contraction. Often initiated or worsened by voluntary movement*
Dystonia
torsional component
brief, intermittent, stereotyped movements associated with urge to make the movement
Tics
*can suppress it for a little but eventually have to do it
Tremor subtypes
- Essential tremor
- Parkinsonian tremor
- Cerebellar tremor
Describe an essential tremor
- Worsens with posture and/or activity– bringing hand torwards faces
- Can be low or high amplitude
- May begin unilaterally or bilaterally
- Worse w/ holding a weight
Describe a Parkinsonian tremor
- Rest tremor, improves with purposeful movement
- “Pill-rolling tremor”, generally 4-6 Hz
- Begins unilaterally in Parkinson’s disease (may be bilateral in other forms of parkinsonism)
Describe a cerebellar tremor tremor
- Occurs at the end of intentional movement** (Intention tremor– gets worse at the end of the initial movement–> test w/ finger to nose test)
- Slow, broad tremor with large amplitude/ “flapping component”
- Often associated with ataxia
Describe the pathophysiology of Parkinson’s
Gradual depletion of dopamine due to progressive loss of dopaminergic neurons in the substantia nigra
**Diminished substantia nigra
Lewy body plaques seen on autopsy
Parkinson’s
Motor sx onset in Parkinson’s is typically begins when
~10 yrs after this degenerative process begins
Possible triggers for the degenerative process of Parkinson’s
- Genetics
- toxin exposure (ie. pesticides, mines, agent orange)
- head trauma.
*The majority of cases are considered idiopathic at this point.
Describe the epidemiology of Parkinsons
- increase w/ age (most over 40)
- M>F slightly
- Genetics
Describe the initial sx of Parkinson’s
- Symptoms begin unilaterally but can progress to contralateral side.
- Symptoms progress slowly over time. Not all patients develop every symptom.
- Motor sx
- Bradykinesia
- Rigidity
- Tremor
- Gait impairment
- REM Sleep disorder (movement in sleep), insomnia
- impaired sense of smell
- Constipation
(8-10 often predate motor sx by many yrs)