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Neurology Flashcards

1
Q

What are the DD for unilateral ptosis

A 
III nerve palsy
Horner's syndrome
Myasthenia gravis
Myotonic dystrophy
congenital
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2
Q

causes of horner’s syndrome

A 
peripheral; 
pancoast tumour
neck sx
cardiothoracic sx
LAP
Central venous cathetrisation
central:
 syringomyelia
demyelination
neck trauma
myasthenia gravis
myotonic dystrophy
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3
Q

what are the complications of ventricular setpal defects?

A 
infective endocarditis
pulmonary hypertension
left ventricular dysfunction
aortic regurgitation
ventricular arrhythmias
Eisenmenger's syndrome
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4
Q

What is the muscle that open the eye?

A

Levator palpebrae superioris muscle, innervated by oculomotor nerve, under the levator is smooth muscle fibres, innervated by cervical sympathetic nerves. Ptosis results fr damage to these nerves or disorder of muscle or neuromuscular junction.

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5
Q

What are signs of oculomotor palsy?

A

Complete ptosis, unilateral,
When pt attempting to look straight ahead, the eye is ‘down and out’, there is weakness of adduction and vertical eye movement
Pupil is fixed and dilated.
If pupillary sparing, consider diabetes or hypertension

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6
Q

What are signs of Horner syndrome

A

Unilateral incomplete ptosis
Smaller pupil, normal reactive to lights
Anhidria
Other signs to localise lesion
Cornea reflex in the Se eye( orbital or retro - orbital lesions)
Weakness and loss of reflexes in the ipsilateral arm ( avulsion injury to the brachial plexus, pan coast tumour of lung apex)
Ipsilateral loss of facial pain and tolerate sensation and contralateral loss of pain and sensation in the trunk and limbs( brainstem lesion)

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7
Q

Ptosis due to myopathy or MG?

A

Ptosis with weakness of extra-ocular muscles and orbicularis oculi consider myasthenia gravis
Fatigability test in eyelid and deltoid muscles
Normal pupils signify disorder of muscle or neuromuscular junction
Senile ptosis has no associated neurological signs
Dystrophia myotonica: frontal balding, cataract, wasting of the masseters, sternomastoids and distal limb muscles.

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8
Q

What are the investigation of myasthenia gravis?

A

Respiratory function test
repetitive stimulation studies

Single fibre EMG looking for jitter
Anti-acetylcholine receptor antibodies
Anti- MuSK antibodies if negatives
Tension test 
cT of chest to exclude thyma
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9
Q

What are three main vision abnormality

A

Abnormality of vision
Abnormality of eye movements
Pupillary abnormality

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10
Q

What are DD of abnormality of vision

A 
Impairment of acuity in one eye
Bilateral hemianopia
Homonymous hemianopia
Upper homonymous quadrantanopia 
Lower homonymous quadrantanopia
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11
Q

What are etiology of impairment of acuity in one eye?

A

Lies in the anterior visual system: the eye( Central retinal artery occlusion, retinitis pigments a) itself or the optic nerve ( optic neuritis or ischaemic optic neuropathy
Optic atrophy includes sub-frontal meningioma, pipuitary tumour, carotid aneurysm, anterior ischaemic optic neuropathy.

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12
Q

lateral medullary syndrome

A

vestibular nuclei
vestibular system: vomiting, vertigo, nystagmus,
inferior cerebellar peduncle Ipsilateral cerebellar signs including ataxia, dysmetria (past pointing), dysdiadokokinesia
lateral spinothalamic tract contralateral deficits in pain and temperature sensation from body (limbs and torso)
spinal trigeminal nucleus & tract ipsilateral loss of pain, and temperature sensation from face
nucleus ambiguus - (which affects vagus nerve and glossopharyngeal nerve) - localizing lesion (all other deficits are present in lateral pontine syndrome as well) ipsilateral laryngeal, pharyngeal, and palatal hemiparalysis: dysphagia, hoarseness, diminished gag reflex (efferent limb - CN.X)
descending sympathetic fibers ipsilateral Horner’s syndrome (ptosis, miosis, & anhydrosis)

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13
Q

5th cranial nerve testing

A

Sense: test light touch and pinprick in ophthalmic, maxillary and mandibular distributions
Motor: messeters (clech your teeth), pterygoids (resistance of chin)

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14
Q

what is light reflex

A

constriction of the pupil in response to light is relayed via the optic nerve and tract, the superior quadrigeminal brachium, the Edinger-Westphal nucleus and its efferent parasympathetic fibres, which terminate in the cilliary ganglion, there is no cortical involvment.

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15
Q

what is accommodation reflex

A

constriction of the pupil with accommodation originates in the cortex (in association with convergence) and is relayed via parasympathetic fibres in the third nerve.

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16
Q

causes of absent light refelx but intact accommodation reflex

A

midbrain lesion,
ciliary ganglion lesion
Bilateralanteriorisualpathway lesions
Parinaud’s syndrome

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17
Q

causes of absent convergence but intact light reflex

A

Cortical lesion

Midbrain lesions

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18
Q

Causes of pupil contrictin

A 
Horner's syndrome
Argyll Robertson pupil
Pontine lesion (often bilateral, but reactive to light)
Narcotics
Pilocarpine drops
Old age
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19
Q

Causes of pupil dilation

A 
Mydriatics, atropine poisoning or cocaine
Thrid nerve lesion
Adie's pupil
iridectomy, lens impalnt, iritis
Post- trauma, deep coma, cerebral death
Congenital
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20
Q

What is Adie’s syndorme

A

lesion in the efferent parasympathetic pathway.
signs:
dilated pupil,
decreased or absent reaction to light
slow or incomplete reaction to accommodation with slow dilation afterwards
decreased tendon reflexes
patients are commonly young women

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21
Q

What is Argyll Robertson Pupil?

A

lesion of the iridodilator fibres in the midbrain
as in syphilis, diabetes mellitus, alcoholic midbrain degenration, other midbrain lesions
Signs:
small, irregular unequal pupil, no reaction to light, prompt reaction to accommodation,

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22
Q

causes of papilloedema

A 
space-occupying lesion
hydrocephalus
benign intracranial hypertension
hypertension (grade IV
central retinal vein thrombosis
cerebral venous sinus thrombosis
high cerebrospinal fluid protein level - Guillain-Barre syndrome
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23
Q

causes of optic atrophy

A 
Chronic papilloedema or optic neuritis
optic nerve pressure or divison
Glaucoma
Ischaemia
Familial
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24
Q

causes of cataract

A 
Old age
endocrne - diabetes mellitus, steroids
hereditary or congenital
Ocular disease - glaucoma
irradiation
trauma
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25
Q

causes of ptosis

A 
with normal pupils
senile ptosis, myotonic dystrophy, ocular myopahty, thyrotoxic myopahty, myasthenia gravis
congenital, fatigue, botulism, snake bite
with constricted pupils:
Horner's syndrome, 
tabes dorsalis
with dilated pupils
third nerve lesion
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26
Q

What is dominant parietal lobe signs and non dominant parietal lobe signs?

A 
AALF orGerstmann's syndrome
A acalculia 
A agraphia -write
L left right disorientation
F finger agnosia (name fingers)
Non dominal 
Dressing apraxia
constructional apraxia
Both lobes:
visual inattention
Sensory inattention
Cortical sensory loss ( loss of agraphaesthesia, two point discrimination, joint position, sense and stereognosis)
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27
Q

What are frontal lobe signs

A

reflexes - grasp, pout, palmar mental
preverb interpretation: “a rolling stone gathers no moss”
smell
Fundi
Gait: gross unsteadiness in walking - the feet typically behae as if glued to the floor, resulting in a hesitant shuffling gait with freezing

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28
Q

what is features of fluent speech (usually receptive, conductive or nominal dysphasia)

A

naming of objects - patients with nominal , conductive or receptive aphasia name objects poorly
repetition - conductive and receptive aphasics cannot repeat
comprehension - only receptive aphasic patients cannot follow commands
reading - conductive and receptive aphasic patients have difficulty reading
writing - conductive aphasic patients have impaired writing( dysgraphia), whereas receptive aphasic patients have abnormal content

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29
Q

what is nonfluent speech (expressive aphasia)

A

naming of objects - poor
repetition - may be possible with great effort, phrase repetition is poor
comprehension - nearnormal (written and verbal commands are followed)
writing - dysgraphia may be present
look for hemiparesis - arm more affected than leg

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30
Q

where is the lesion of conductive aphasia and nominal aphasia

A

conductive aphasia: arcuate fasciculus
nominal aphaisa: angular gyrus (temporallobe)- small localised lesion
other causes of nominal aphaisa: encephalopathies, pressure effects form space -occupying lesion, recovery pahse from any dysphasia

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31
Q

what are signs of hereditary motor and sensoryneuropahty charcot- Marie-tooth disease

A

pes cavus (short, high-arched feet with hammer toes)
distal muslce atrophy owing to peritpheral nerve degeneration, not usually extending above the elbows or above the middle one third of the thighs
absent reflexes
slight ot no sensory loss in the limbs
thickened nerves
optic atrophy

32
Q

Median nerve lesion (C6 - T1)

A 
LOAF
lateral two lumbricals
Opponens pollicis
Abductor pollicis brevis
Flexor pollicis brevis 
clinical features:
1. loss of abductor pollicis brevis with a lesions at or above the wrist - pen touching test: with the hand flat, ask the patient to abduct the thumb vertically to touch your pen
2. loss of flexor digitorum sublimis with a lesion in or above the cutibalfossa - Ochsner's clasping test: ask the patient to clasp the hands firmly together - the infex finger on the affected side fails to flex
33
Q

features of ulnar nerve (C8 - T1 ) lesion

A

wasting of the intrinsic muscles of the hand (exept LOAF muscles)
weak finger abduction and adduction (lesion of interosseous msucles)
ulnar claw-like hand (note: a higher lesion causes less deformity, as an aboe the elbow lesion als causes loss of flexor digitorum profundus)
Froment’s sign: ask the patient to grasp a piece of paper between the thumb and lateral aspect of the forefinger with each hand - the affected thumb will flex (loss of thumb adductor)
sensory loss over the little and medial half of ring finger

34
Q

causes of wasting of the small muscles of the hand

A

nerve lesion: meidan and ulnar nerve lesions, brachial plexus lesions, peripheral motor neuropahty
Anterior horn cell disease: motor neurone disease, polio, spinal muscular atrophies
Myopathy: dystrophia myotonica, distal myopathy
Spinal cord lesions: syringomyelia, cervical spondylosis with compression of C8 segment
Trophic disorders: arthropathies, ischaemia, including vasculitis, shoulder- hand syndrome.

35
Q

what are features of femoral (L2,3,4) lesion?

A

weakness of knee extension(l3,4)
slight hip flexion weakness (L2,3)
preserved adductor strength
loss of knee jerk (L3,4, quadricept muscle)
sensory loss involving the inner aspect of the thign and leg.

36
Q

what are features of sciatic nerve(L4,5, S1,2)

A

weakness of knee flextion (hamstrings involved)
loss of power of all msucles below the knee causing a foot drop,
knee jerk intact
loss of ankle jerk and plantar response (s1)
sensory loss along the posterior thigh and total loss below the knee.

37
Q

What are features of common peroneal (lateral popliteal) nerve (L4,5,S1)lesion

A

foot drop and loss of foot eversion only

sensory loss over the dorsum of the foot.

38
Q

what are features of lateral cutaneous nerve of the thigh lesion?

A

meralgia paraesthetica is caused by compression of this nerve, which may result in sensry loss and or hyperaesthesia over the lateral aspect of the thigh, but no motor loss

39
Q

what are causes of foot drop?

A 
common peroneal nerve palsy
sciatica nerve palsy
lumbosacral plexus lesion
L4,L5 root lesion
peripheral motor neuropathy
distal myopathy
motor neurone disease
Precentral gyrus lesion
(ifthere is a foot drop, test the ankle jerk carefully. as a very tough rule of thumb, if it is absent, an S1 lesion should be suspected; if it is normal, a common peroneal palsy should be considered, if it is increased, an upper motor neurone lesion is likely.
40
Q

Assessment of the paraplegic patient

A

is there a sensory level? a. cord compression, transverse myelitis, anterior spinal artery occlusion, intrinsic cord lesion, multiple sclerosis
backexamination
arm involvement: consider: cervical spondylosis, syringomyelia, motor neuron disease, multiple sclerosis
Cranial nerve lesions involved? consider motor neurone disease, multiple scelrosis
Periphearl neuropahty? consider: vitamin B12 deficiency, Friedreich’s ataxia, carcinoma, hereditary spastic paraplegia, syphilis
(intracranial lesions cause paraplegia in extension only, where spinal cord lesions causes paraplegia in flexion and extension (flexor reflexes are released withspinal lesions)

41
Q

What arefeatures of vitamin B12 deficiency?

A

symmetrical posterior column loss (vibration and position sense), causing an ataxic gait
symmetrical upper motor neurone signs in the lower limbs with absent ankle reflexes, knee reflexes may be absent or, more oftenexaggerated
peripheral sensory neuropathy

42
Q

cuases of an extensor plantar response plus absent ankle jerk include:

A

1 subacute combined degeneration of the cord (vit B12 deficiency)
conus medullaris lesion
combination of an upper motor neurone lesion with cauda equina compression or peripheral neuropathy
syphilis
Friedreich’s ataxia
diabetes mellitus

43
Q

What are features of Brown-sequard syndrome

A

Motor changes: upper motor neurone signs below the hemisection on the same side as the lesion, lower motor neurone signs at the level of the hemisection on the same side
Sensory changes: pain and temperature loss on the opposite side of the lesion, vibration and proprioception loss on the same side, light touch is often norma, there may be a band of sensory loss on the same side at the level of the lesion.
common causes:
multiple sclerosis, angioma, Glioma, trauma, myelitis, postradiation myelopathy

44
Q

Causes of dissociated sensory loss (usually indicates spinal cord disese,but may occur with peripheral neuropahty

A
  1. Syringomyelia
  2. Brown-sequard syndorme
    ANterior spinal artery thrombosis
    Lateral medullary syndorme (contralateral to the other signs)
    Peirpheral neuropathy (diabetes mellitus, amyloid)
45
Q

what are common causes of dorsal column (vibration and proprioception) loss only?

A

subacute combined degeneration
Brown -Sequard syndrome
Spinocerebellar degeneration( Friedreich’s ataxia)
Multiple scelrosis
Sensoryneuropathy or ganglionopahty
peripheral neuropathy form diabetes mellitus or hypothyroidism

46
Q

What are features of synrongomyelia?(a central cavity in the spinal cord)

A

loss of pain and temperature over the neck, shoulders and arms(‘cape’ distribution)
Amyotrophy(weakness, atrophy and areflexia) of the arms
upper motor neurone signs in the lower limbs

47
Q

Differenciation of motor neurone disease

A

Syringomyelia - sensory loss and presence of HOrner’s syndorme
cervical myelopathy - bulbar and sensory signs
spinal cord tumour- senosry loss
CIDP - raised cerebrospinal fulid
Polyneuropathy - sensory or autonomic dysfunciton
spinal muscular atrophy
spinobulbar muscular atrophy
old poliomyelitis - progressive wasting disease wtih prominent fasciulations

48
Q

causes of fasciculations

A 
after exercise
hypokalaemia and hypomagnesaemia
thyrotoxic myopathy
cervical spondylosis
syringomyelia
hereditory motor and sensory neuropathy
drug( salbutamol, litium)
spinal msucular atrophy
neuralgic amyotrophy
syphilitic amyotrophy
49
Q

treatment of myasthenia gravis

A

symptomatic :
1. anticholinesterases, Pyridostigmine , pottasium supplemnt and potassium sparing diuretics may give additional improvememtn
2. avoid drugs: gentamicin, quinidine , procainamide, streptomycin
3. myasthnic crisis, precipitated by infection,
4. cholinergic crisis
disesae - suppressing
1 steroids
2. immunosuppressive drug: azathioprine, cyclospine, mycophenolate
3. Thymectomy
4. plasmapharesis
5. rituximab
prognosis is good; 50% of patients have a remission, although 5-10% die from respiratory failure

50
Q

Differential diagnosis of myasthenia gravis?

A 
Lambert-eaton myasthenic syndrome
Miller- Fisher syndrome
Mitochondiral myopathy
Snake bites
Botulism
51
Q

causes of palatal weakness?

A 
Common causes of palatal weakness:
Brainstem injury
myasthenia gravis
EATON lambert syndrome
muscular dystrophy
down syndrome
Less common causes:
thrombocytopenia
velocardiofacial syndrome
52
Q

treatment of motor neuron diasease

A

Symptoms:
1. drooling - anticholinergic drugs, tricyclic anti-depressant, hyoscine pathces, glycopyrrolate, radiotherapy to parotids and home suciton devices
2. dysphagia- dietary advice and consider percutaneous endoscopic gastrostomy
3. communication difficulties - speech and language therapist
4. pathological laughing or crying (emotional lability) -amitriptyline, lithium and levodopa
5 Fasciculations and msucle cramps - magnesium, diazepam, carbamazepine and phenytoin
6. spasticity - physiotherapy and drugs, baclofen,
7. Limb weakness - splints or neck support and physiotherapy to aid posture
8. respiratory symptosm - non invasive respiratory support can be considered
9 Depression - consdier amitriptyline or SSRI
10. pain - analgeisa, physiotherapy and cccupational therapy
Disease modifying treatments: Riluzole

53
Q

what are common causes of cerebellar syndorme?

A 
demyelination
alcoholic cerebellar degeneration
posterior fossa space occupying lesions
brainstem lesions
Friedreich's ataxia
paraneoplastic cerebellar degeneration
spinocerebellar degeneration
hypothyroidims
arnold -chiari malformation
drugs: phenytoin, carbamazepine, lithium, phenobarbitone
54
Q

Complete lesion of brachial plexus ?

A

a. lower motor neurone signs affect the whole arm
b. sensory loss (whole limb)
c. Horner’s syndrome ( an important clue, but only if the lesion is proximal in the lower plexus)
remember always to feel for axillary lymphadenopathy at the end of exam

55
Q

Signs of upper trunk (C5, C6) lesion

A

loss of shoulder movemnt and elbow flexion

sensory loss is presnet over the lateral aspect of the arm and forearm, and over the thumb.

56
Q

the proximal muscles of the upper limb

A

Deltoid: shoulder abduction, axillary nerve, C5/6 roots
biceps: elbow flexion; musculocutanous nerve, C5/6 roots
tricepts: elbow extension, raidal nerve C7/8
brachioradialis: elbow flexion with the thumb pointing to the shoulder; raidal nerve C5/6 roots
supraspinatus: first 20 of shoulder abduction, suprascapular nerve, C5/6
infraspinatus: external rotation at the shoulder; suprascapular nerve; C5/6 roots
Trapezius: shoulder rotation at the shoulder; spinal accessory nerve: C3/4
serratus anterior: scapular fixation and rotation; long thoracic nerves; C5/6/7

57
Q

weakness confined to deltoid?

A

this can not be C5/6 root lesion for bicept and brachioradialis are spared. this is axillary nerve lesion, reflexes will be normal. an area of sensory loss over the deltoid.

58
Q

weakness of deltoid, bicepts and branchioradialis, with normal power in the other muscles?

A

C5/6 cord lesion: the refelxes at the level of the lesion- biceps and brachioradialis are absent while triceps and the lower limb refelxes are increased. test tone and power in the lower limbs and look for a sensory level at C5.
C5/6 root or plexus lesion: biceps and brachioradialis refelxes are absent, but triceps reflex and leg reflexes are normal. the point at which these nerves have been damaged is determined by testing muslces. 1st branch: serratus anterior controll stabling scapula, 2; supraspinatus and infraspinatus to abduction and external rotation. 3. axillary nerve to control deltoid, musculocutaneous nerve to control biceps, radial nerve to control brachioradialis.

59
Q

Radial nerve lesion C5-C8

A

wrist and finger drop (wrist flexion normal)
triceps loss if leson is above the spiral groove
sensory loss over the antomical snuff box
finger abduction appears to be weak because of the difficulty of spreading the fingers when they can not be straightened
brachioradialis is the key msucle to test in suspected radial nerve palsy

60
Q

median nerve (C6-T1) lesion

A

the nerve supplies all msucles on the front of the forearm except flexor carpi ulnaris and half of flexor digitorum profoundus and short muslces of LOAF: lateral two lumbricals, opponents pollicis, abductor pollicis brevis, flexor pollicis brevis
clincial features:
1. loss of abductor pollicis brevis with a lesion at or above the wrist - pen touching test
2. loss of flexor digitorum sublimis with a lesion in or above the cubital fossa

61
Q 
ulnar nerve (C8 T1)
Flexor digitorum profoundus, action: flex hand and both interphalangeal joints. By median and ulnar nerve
A

wasting of the intrinsic muscles of the hand
weak finger abductions and adductions (loss of interosseous muscles)
ulnar claw-like hand ( note: a higher lesion causes less deformity, as an above the elbow lesion also causes loss of flexor digitorum profundus.)
Froment’s sign: ask the patient to grasp a piece of paper between the thumb and lateral aspect of the forefinger with each hand - the affected thumb will flex (loss of thumb adductor).
sensory loss over the little and medial half of rign finger.

62
Q

wasting of the small muscles of the hand

A 
1. nerve lesions:
median and ulnar nerve lesions, 
branchial plexus lesions
peripheral motor neuropahty (inc. hereditary motor and sensory neuropahty)
2. Anterior horn cell disease;
motor neurone disease, polio, spinal muscular atrophies
3. myopathy:
dystrophia myotonia
distal myopathy
4. spinal cord lesions:
syringomyelia, cervical spondylosis, tumor
5. Trophic disorders:
ischaemia, including vasclulitis
arthropathies(disuse)
63
Q

Femoral nerve (L2,L3, L4) lesions

A
  1. weakness of knee extension (quadriceps paralysis)
  2. slight hip flexion weakenss
  3. preserved adductor strength
  4. loss of knee jerk
  5. senosry loss involving the inner aspect of the thigh and leg.
64
Q

Sciatic nerve (L4,L5, S1, S2) lesions

A
  1. weakness of knee flexion(hamstrings involved)
  2. loss of power of all muscles below the knee causing a foot drop
  3. knee jerk intact
  4. loss of ankle jerk and plantar response
  5. sensory loss along the posterior thigh and total loss below the knee
65
Q

Common peroneal nerve (L4,L5 and S1) lesion

A
  1. foot drop and loss of foot eversion only

2. sensory loss (minimal ) lver the dorsum of the foot.

66
Q

Common peroneal nerve (L4,L5 and S1) lesion

A
  1. foot drop and loss of foot eversion only

2. sensory loss (minimal ) over the dorsum of the foot.

67
Q

causes of foot drop?

A 
common peroneal nerve palsy
sciatic nerve palsy
lumbosacral plexus lesions
L4,L5 root lesion
Peripheral motor neuropathy
distal myopathy
motor neurone diseae
precentral gyrus lesions
68
Q

what are signs of medial pontine syndrome (has CN V, VI, Vii, VIII)

A

corticospinal tract cause contralateral hemiparesis
contralateral Posterior columne-medial lemniscus pathway loss ( loss localized senstion of fine touch, vibration, two -points discriminaiton and propioception)
abducence nerve palsy (ipsilateral lateral rectus muscle paralysis)abducence nerve lesion localized lesion in inferior pons

69
Q

what are signs of mid brain infarction?

A

CN III palsy with eye movement disorder,
vertical gaze paresis
pure motor hemiparesis
four limbs ataxia due to unilateral lesion

70
Q

anatomy of mid brain and funciton

A

cranial nerve III , IV and V
integration centres for auditory pathway
integrate the visual pathways and also are involved in somatic reflexes that are caused by visual cues
substantia nigra nuclei are involved in the control of voluntary movement

71
Q

what are signs of lateral pontine syndrome?

A

Ipsilateral cerebellar ataxia due to involvement of cerebellar tracts
Contralateral hemiparesis due to corticospinal tract involvement
Variable contralateral hemihypesthesia for pain and temperature due to spinothalamic tract involvement

72
Q

what are the causes of dissociated sensory loss?

A

Syringomyelia
anterior spinal artery occulsion( espeially in T8-L2, the spinothalamic and corticospinal tracts are affected, and hte posterior columns are sparted.
small fibre neuropathies ( impairment of small calibre sensory nerve fibres, inluding cold, pain and autonomic and unmyelinated C fibres (warmth). vibration and propioception (large fibres) are relatively preserved.

73
Q

what are pahtophysiology of Friedreich’s ataxia?

A 
Loss of propioception and vibraiton sense( degeneration of the posterior columns)
Hyporeflexia (loss of large nerve fibres in the dorsal root ganglia)
cerebellar ataxia (degeneration of lateral and ventral spinocerebellar tract
Pyramidal weakness and extensor plantar responses ( degeration of the corticospinal tracts (these tracts are relatively spared down to the cervicomeduallary junction, after which they are degenerated)
74
Q

what are signs of Thurner’s syndrome

A 
short stature
square chest
webbed neck
high arched palate
short fourth metacarpals.
complications:
cardiac; bicuspid aortic valve, coarctation of the aorta, HTN
diabets:
hyothyroidism
hypogonadism
75
Q

Differenciation of postural hypotension

A

autonoic neuropathy
alcoholic neuropathy
acute inflammatory demyelinationg polyradiculoneuraphy
chronic inflammatory demyelinationg polyradiculopathy
charcot marie tooth and other herediry motor and sensory neuropathy
diabetic neuropathy
parkinson and parkinsonism
paraneoplastic autonomic neuropathy
HIV associated acute /chronic demyelinatiing

76
Q

Posterior circulation stroke signs

A

4DS: dysarthria, dysphagia, diplopia, dizziness
2Cs: crossed signs, cerebellar signs, heminopia alone or in combination with any o fthe above.

Short case (8 decks)

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