midterm review Flashcards
increased tone leading to spastic paralysis
UMN
decreased tone leading to a flacid paralysis
LMN
is the anterior horn cell only found in the spinal cord?
YAAAS
which tract crosses in the spinal cord
spinothalamic tract
tell me about suspended sensory loss
when there is something wrong with the anterior white commissure causing a loss of pain and temp. at one or couple of segments in the body
Brown sequard syndrome… what is wrong with it?
- contralateral pain and temperatures (spinothalamic) - ipsilateral issues with position, vibration (dorsal column pathway) and motor (CST)
a motor or sensory level involvement means what?
that it is a spinal cord disease because the spinal cord is segmented
Sensory levels:
T2 =
T4 =
T10 =
L1 =
L3 =
L5 =
S4-S5 =
T2 = clavicle
T4 = nipple line
T10 = umbilicus
L1 = inguinal crease
L3 = medial thigh
L5 = lateral calf
S4-S5 = perianal (“saddle”) area
Muscle innervation
Biceps brachii =
Triceps =
Intrinsic hand muscles =
Quadriceps femoris =
Gastrocnemius =
Biceps brachii = C5,
Triceps = C7
Intrinsic hand muscles = C8
Quadriceps femoris = L3
Gastrocnemius = S1
In spinothalamic tract, sacral fibers are _______, cervical fibers are ______
In spinothalamic tract, sacral fibers are lateral, cervical fibers are medial
sacral sparing is considered a
intrinsic disease
syringomyelia
suspended sensory loss of pain and temp. leads to weakness and atrophy
ALS
combined UMN and LMN
Tabes Dorsalis
Dorsal column
Subacute combined degeneration
B12 deficiency dorsal column and corticospinal tracts
spinocerebellar degneration–> Friedreich’s ataxia
- dorsal column - spinocerebellar - CST
- spinal muscular atrophies - motor neuron disease -local damage, trauma - ischemia, tumors and infections
diseases of motor neurons
- axonal degneration - segmental demyelination
diseases of peripheral nerves
- MG
- Eaton-Lambert syndrome
Diseases of NMJ
- destructive myopathies
- dystrophies
- polymyositis
- dermatomyositis
primary muscle disease
mitochondria, glycogen lipids, ion channels, deamin related proteins
disorders of intracellular organelles, structural proteins, and enzymes
dying back
axonal neuropathy
Axonal neuropathies
- affects proximal or distal?
- most common causes?
- what do we see on NCV?
- distal - toxic and metabolic -decreased amplitudes
charcot-marie-tooth type 1 is a
herditary,chronic demyelinating neuropathies
example of an acute demyelinating neuropathy
guillain-Barre
Tell me about Guillain-Barre?
- causes?
- motor < or > sensory
- CSF increased or decreases? what about cell count?
- fast or slowed conduction velocity
- tx,
- what is more rapid in recovery? remyelination or axonal regeneration
- autoimmune disorder after a viral or bacterial illness
- motor > sensory
- CSF increased with normal cell count
- slowed conduction velocity
- tv.: plasma exchange but no steroids
- recovery by remyelination
Chronic inflammatory demyelinating neuropathy can be treated by
steroids
_____ mediated in chemical transmission
ACh
Myasthenia Gravis:
- what is happening here?
- what is usually present in terms of symptoms?
- common system affected
- how do we dx?
- 10% of cases have
- tx?
- post-synaptic autoimmune mediated AChR dysfunction
- fatigable weakness is usually present
- most common system affected is ocular
- tensilon test, Ab levels
- 10% have thymomas
- acetylhonesterase inhibitors or immunosuppressive medications
lambert- eaton syndrome
- what is it?
- what do we see?
- tell me about the reflexes?
- common paraneoplastic syndrome
- tx?
- autoimmune presynaptic VGCC dysfunction
- slowly progressive proximal weakness with dry mouth
- hyporeflexic
- small cell lung cancer
- prednisone, 3,4diam
what are these features suggestive for?
- proximal distribution of weakness
- symmetric muscle weakness
- normal or enlarged muscles
- deep tendon reflex reductions that parallel muscle strength
myopathy
these features really do not fit with ________
- UMN
- distal weakness
- fasciculations
- tremor
- sensory abnormalities
- fatigable muscle weakness
- early loss of deep tendon relfexes
myopathy
what type of muscle enzyme testing we can do to dx myopathies?
creatine kinase
dx that involves finger flexors and quads
inclusion body myositis
inflammatory myopathies [3]
what do all three show?
what about tx?
- polymyositis
- dermatomyositis
- inclusion body myositis
- elevated CK
- PM and DM respond to immunosuppresive tx. but IBM does not
inherited muscle disease largely due to abnormal structural muscle proteins
muscular dystrophies
muscular dystrophies diseases?
[3] how are two inherited?
- Duchenne’s
- Becker’s
- fascioscapulohumeral dystophy
Duchenne’s/ Becker’s are x-linked but beckers’ is less severe as in-frame mutation
broad group of inherited disorders of muscle energy metabolism largely presenting with exercise intolerance
metabolic myopathies
Cranial nerve determines level:
midbrain =
pons =
medulla =
midbrain = III,IV
pons = V, VI, VII, VIII
medulla = IX, X, XI, XII
medial disease localization of the brainstem
CST and medial lemniscus
lateral disease localization of the brainstem
Spinothalamic and descending V
Medial cranial nerves
- derived from ____ ______ column
III =
VI =
XII =
Medial cranial nerves:
- derived from somatic motor column
III = midbrain
VI = pons
XII = medulla
Lateral cranial nerves - ______ and _____ arch muscles
IX, X, XI =
VII, VIII, V =
Lateral cranial nerves - sensory and branchial arch muscles
IX, X, XI = medulla
VII, VIII, V = pons
lateral brainstem syndromes:
Contralateral loss of pain and temperature in body: ___________
Ipsilateral loss of pain and temperature in face: ______________
Laterally exiting cranial nerves to branchial arch muscles:
Medulla-
Lower pons-
Upper pons-
Contralateral loss of pain and temperature in body: Spinothalamic tract
Ipsilateral loss of pain and temperature in face: Descending nucleus of V
Laterally exiting cranial nerves to branchial arch muscles:
Medulla- nucleus ambiguous
Lower pons- facial nerve
Upper pons- trigeminal nerve (main sensory, motor)
lateral medullary syndrome:
Sensory: [2]
Motor [1]
Other [2]
Sensory: pain and temp
- Ipsilateral face
- Contralateral body Motor
- Ipsilateral palatal weakness (nucleus ambiguus); contralateral uvulal deviation
Other - Ipsilateral
Horner’s syndrome - Ipsilateral dyscoordination/ataxia
What is the difference between the lateral pontine syndrome and lateral medullary syndrome?
there is different motor components in the pontine syndrome there is facial weakness due to CN VII affected lateral medullary syndrome affects the nucleus ambiguus so we see palate weakness and contralateral uvula deviation
Medial brainstem syndromes:
Contralateral hemiparesis:
involvement of somatic motor nerves exiting medially:
Medulla =
Pons =
Midbrain =
Contralateral loss of position and vibratory sense (which levels of brainstem)
Contralateral hemiparesis:
Corticospinal tract Ipsilateral
involvement of somatic motor nerves exiting medially:
Medulla = XII
Pons = VI
Midbrain = III
Contralateral loss of position and vibratory sense: Medial lemniscus (medulla, lower pons)
medial medullary syndrome:
Sensory what type of sensory and where is the deficit?
Motor (be specific in what happens)
Sensory (touch/vibration)
- Contralateral body Motor
- Ipsilateral tongue weakness (CN XII); deviates ipsilaterally
- Contralateral weakness (spares face)
medial pontine syndrome and medial medullary are very different.
What happens in medial pontine syndrome?
we know that in medial medullary we are going to have a sensory loss of pain and temp contralateral in the body and ipsilateral in the face. we are also going to see tongue deviated to the week side and contralateral body weakness
For medial pontine syndrome:
- there is loss of touch and vibration in contralateral body
- contralateral weakness and will include face if above facial nucleus ipsilateral weakness
- ipsilateral eye abduction weakness CN VI
what the heck is ventral midbrain syndrome? please be specific of what happens with the involved CN
- there will be contralateral weakness of the body and ipsilateral weakness of the face
- ipsilateral CN III.
this leads to a deviated down and out, dilated and unreactive pupil
Talk to me about the importance of the cerebellopontine angle:
what CN nerve signs are involved?
early vs late what type of symptoms show up later?
- extrinsic compression of tumors
- begins with CN VIII with vestibular before cochlear
- later involvement of V and VII later when the tumor is bigger it starts to affect:
- middle cerebellar peduncles leading to ataxia
- CST leading to hemiparesis
nerves in the cavernous sinus? what is the artery?
CN III, IV, VI, V1 and V2 CN VI closest to the ICA
basilar artery occluions involves what motor and sensory tract?
what is variable?
what happens if the reticular system is affected? or not?
- bilateral hemiparesis
- bilateral sensory loss
- variable CN nerve signs
- reticular system:
- if involved: coma
- if spared- “locked- in- syndrome”
normal lateral gaze involves
CN 6 and 3
conjugate nerve palsy
lesion to CN6
internuclear opthalmoplegia
lesion to MLF
one and a half syndrome
lesion to both CN 6 and MLF
input to the cerebellum all have to pass through the granule cell layer
false all except from inferior olives
purkinje cells are found deep to the
cerebellar nuclei
how does inferior olive project directly to purkinje cells?
climbing fibers
tell me about the inferior cerebellar peduncle. where is it found? why is it important?
found in medulla it receives input from all except cerebral cortex
tell me about the middle cerebellar peduncle. where is it found? why is it important?
found in the pons receives only imputs from cerebral cortex (pontocerebellar)
tell me about the superior cerebellar peduncle. where is it found? why is it important?
found in the midbrain receives output from cerebellar cortex
vestibulocerebellum or also flocculonodular is involved in
balance and oculomotor control
spinocerebellum (vermis) involved in
truncal incoordination and leg incoordination
neocerebellum (lateral hemispheres) involved in
upper limb ataxia/incoordination
Dysdiadochokinesis-
trouble performing rapidly alternating movements
tumors, infarct and hemorrhages are unilateral or bilateral?
unilateral
cerebellar degenerations are unilateral or bilateral
bilateral
what does dopamine do in the direct pathway? what about indirect?
direct- stimulates indirect- inhibits
subthalamic nucleus is part of the direct or indirect pathway
indirect
where is a loss of dopamine producing cells in substantia nigra located
pars compacta
which part of the basal ganglia does HNT affect
caudate nucleus, cortex
describe the movement: tremor
oscillatory
describe the movement:
myoclonus
jerky
describe the movement:
chorea
random
describe the movement:
hemiballismus
violent
describe the movement:
dystonia
sustained
describe the movement:
tics
stereotyped but can be suppressible
where is this found?
substantia gelatinosa
all
where is this found?
clarke’s nucleus
T1-L2
where is this found?
intermediolateral column
T1- L3
where is this found?
Parasympathetic nucleus
S2-S4
where is this found?
Acessory nuleus
medulla- C5
What is most medial and lateral in the somatotopic organization of Dorsal column Pathway?
Most medial- sacral most lateral is cervical
the spinocerebellar are _____ in the body
ipsilateral
centers for regulation of HR and respiration found in
medulla and Pons
reticular activating system found in
rostral pons and midbrain
what level is this at?
what level is this at?
Cerebellum blood supply
- posterior inferior cerebellar artery (PICA)
- anterior inferior cerebellar artery (AICA)
- superior cerebellar artery (SCA)
Medulla blood supply
- vertebral arteries
- PICA
Pons blood supply
- Basilar artery
- AICA
Midbrain blood supply
- posterior cerebral artery (PCA)
- Superior Cerebellar artery
