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Nervous system disorders Flashcards

1
Q

DDx for polyneuropathies

A

Diabetes mellitus.

Paraneoplastic sensory neuropathy.

Nutritional neuropathy.

Multiple myeloma.

Amyloid.

Dominantly inherited sensory neuropathy.

Toxic (arsenic, thallium, metronidazole).

AIDS-associated neuropathy.

Tangier disease.

Fabry’s disease.

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2
Q

what is polyneuropathy

A

– diffuse, symmetrical disease.

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3
Q

what is mononeuritis multiplex?

A

several individual nerves are afected

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4
Q

causes of mononeuritis multiplex

A
  1. Diabetes
  2. Wagner’s granulomatosis
  3. RA
  4. Polyarteritis nodosa
  5. Sarcoidosis
  6. Amyloidosis
  7. Carcinomatosis
  8. Leprosy
  9. Neurofibromatosis
  10. HIV, HCV
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5
Q

what is mononeuropathy?

A

a single nerve is affected

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6
Q

causes of mononeuropaty

A

Compressive neuropathy (carpal tunnel, meralgia paresthetica).

Trigeminal neuralgia.

Ischemic neuropathy.

Polyarteritis nodosa.

Diabetic mononeuropathy.

Herpes zoster.

Idiopathic and familial brachial plexopathy

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7
Q

what is guillain barre?

A

(acute idiopathic postinfectious polyneuritis). Most common acute polyneuropathy (3/100 000 a year), monophasic – does not recur. Paralysis follows 1-3 weeks after infection w/ Campylobacter jejuni or CMV or other. Molecular mimivry is the possible mechanism.
Primarily affects motor neurons of the ventral roots of peripheral nerves, produces LMN symptoms
1. characterised by demyelination and oedema
2. upper cervical root (C4) involvement is common → respiratory paralysis
3. caudal cranial nerve invlvement with facial diplegia in 50%
4. elevate protein elvels may cause papilloedema
5. protein level in CSF elevated but without pleocytosis

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8
Q

aetiologies of predominantly sensory neuropathy:

A

diabetes mellitus, alcohol, drugs, vitamin deficiencies (B1, B12), uraemia
Drugs: amiodarone, gold, isoniazind, metronidazole, nitrofurantoin, phenytoin, vinca alkaloids.

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9
Q

aetiologies of predominantly motor neuropathy

A

Guillain-Barre syndrome, malignancy, CMT disease, porphyria, lead poisoning

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10
Q

what is Charcot Marie Tooth disease:

A

A hereditary sensory and motor neuropathy, aka peroneal muscle atrophy
Usually starts at puberty with foot drop and weak legs. Peroneal muscles are first to atrophy, with upper limb signs appearing at later stage. There is muscle wasting, pec cavus, bilateral for droop (high-stepping gait). Reflexes often absent. sensory loss is variable. Most commonly autosomal dominant inheritance.

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11
Q

Carpal tunnel syndrome:

A
  1. Wasting of thenar eminence
  2. Weakness of LOAF (lumbricals, opponens pollicis, abductor pollicis brevis, flexor pollicis brevis)
  3. Sensory loss over the lateral 3.5 digits
  4. Maximal wrist flexion for 1 min may elicit symptoms (Phalen’s test)
  5. Tapping over the nerve at wrist induces tingling (Tinel’s test)
  6. Look for a scar from carpal tunnel release surgery and evidence of diabetes, hypothyroidism, acromegaly, rheumatoid arthritis.
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12
Q

ulanr nerve palsy:

A
  1. Wasting of hypothenar eminence, claw hand, huttering on the dorsal aspect of the hand.
  2. Also look for wasting in the medial aspect of the forearm (note low/high lesions, hand less clawed in high lesions)
  3. Weakness of abduction and adduction (test Froment’s sign) of the fingers and adduction of the thumb.
  4. Sensory loss over medial 1.5 digits.
  5. Look for scars (fracture dislocation) and osteoarthrosis at the elbow
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13
Q

radial nerve palsy

A
  1. Wrist drop, weakness of wrist extension. If the wrist is passively extended, intrinsic muscles of the hand should be intact.
  2. Impaired grip strength
  3. Sensory loss over first dorsal interosseous.
  4. Look for scars at the elbow, note if the patient uses crutches.
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14
Q

common peroneal nerve palsy

A
  1. Foor drop, high-stepping gait
  2. Weakness of dorsiflexion and eversion of the foot
  3. All reflexes intact
  4. Sensory loss over the lateral dorsum of the foot
  5. Look for evidence of compression around the fibular neck
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15
Q

DDx for foot drop:

A
  1. Common peroneal nerve palsy
  2. Peripheral neuropathy (especially CMT disease)
  3. Sciatic nerve palsy
  4. L4/5 radiculopathy
  5. Lumbosacral plexopathy
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16
Q

Causes of wasting of the small (intrinsic) muscles of the hand

A

Resembles an ulnar nerve lesion but with thenar wasting and weakness also.
Causes:
1. Anterior horn cells disease, eg poliomyelitis
2. Radiculopathy eg trauma, prolapsed disc
3. Plexopathy eg brachial plexus injury, pancoast’s tumour, cervical rib
4. Peripheral nerve lesions

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17
Q

LMN SIGNS

A 
Weakness 
Wasting 
Hypotonia 
Reflex loss 
Fasciculation 
Fibrillation potentials (EMG) 
Muscle contractures 
Trophic changes in skin and nails
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18
Q

UMN (AKA PYRAMIDAL) SIGNS

A 
Drift of upper limb 
Weakness with characteristic distribution 
Changes in tone: flaccid-spastic 
Exaggerated tendon reflexes 
Extensor plantar response 
Loss of skilled finger/toe movements
 Loss of abdominal reflexes
 No muscle wasting 
Normal electrical excitability of muscle
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19
Q

ventral spinal artery occlusion leads to

A

Often at T8 level (watershed). Infarction of anterior 2/3 of spinal cord, spares dorsal columns:
Lateral corticospinal: bilateral spastic paresis + pyramidal signs.
Lateral spinothalamic: bilateral loss of pain, temperature a segment below the lesion.
Anterior spinothalamic: bilateral loss of pressure, crude touch
Hypothalamospinal tract at T2 and above: bilateral Horner’s syndrome
Ventral horns: bilateral flaccid paralysis
Corticospinal tracts to PNS at S2-S4: loss of voluntary bladder, bowel control

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20
Q

subacute combined cord degeneration

A

aka psoterior sclerosis
Deficiency in intake (or metabolism) of vitamin → degeneration in the dorsal and lateral white columns.
Dorsal columns: bilateral loss of fine touch, proprioception and vibration.
Lateral corticospinal: bilateral spastic paresis + pyramidal signs.
SPinocerebellar tracts: bilateral limb ataxia.

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21
Q

brown-sequard syndrome

A

Hemisection of the spinal cord: injury, syringomyelia, spinal cord tumour, or hematomyelia.
Dorsal columns: ipsilateral loss of fine touch, proprioception and vibration.
Lateral spinothalamic: contralateral loss of pain, temperature a segment below the lesion.
Anterior spinothalamic: ipsiateral loss of pressure, crude touch
Lateral corticospinal: ipsilateral spastic paresis + pyramidal signs.
Hypothalamospinal tract at T1 and above: Ipsilateral Horner’s syndrome.
Ventral horns: ipsilateral flaccid paralysis (LMN in the segment of the lesion)

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22
Q

syringomyelia

A

Central cavitation of spinal cord. Frequent,y associated with Arnold-Chiari malformation.
Ventral white comissure (spinothalamic): bilateral loss of pain and temperature at several segmental levels
Touch, pressure, vibration and position sense usually retained (dissociated anesthesia)
Muscle wasting in hand, forearm
Ventral horns: LMN, flaccid paralysis
Brainstem signs as the syrinx extends into the brainstem (syringobulbia) – tongue atrophy, bulbar palsy, Horner’s, impaired facial sensation.

23
Q

causes of spinal cord compression

A

Spinal cord Tumours
Extramedullary (meningioma, neurogibroma)
Intramedullary (ependymoma, glioma)
Vertebral body destruction by bony metastases eg from prostate
Disc and vertebral lesions
- Chronic degenerative and acute central disc prolapsed
- Trauma
Inflammatory
- Epidural abscess
- TB (commonest in 3rd world)
Epidural haemorrhage/haematoma

24
Q

corticospinal (pyramidal system)

A
  • From cortex to lower motor neurons of brainstem (corticobulbar) and spinal scord (corticospinal)
  • Travels via internal capsule
  • At pyramidal decussation, 85% of fibres cross over to lateral corticospinal tract. 15% remain ipsilateral in anterior corticospinal tract.
  • Purposive, skilled, intricate, strong and organised movements. Defective function
25
Q

sx of corticospinal lesions

A

• Sx: loss of skilled voluntary movement, spasticity and reflex change →↑ +/- clonus
o Pyramidal drift of outstretched arms with eyes closed
o Lesion above decussation causes contralateral weakness
o In the upper limb – flexors remain stronger than extensors
o In the lower limb, extensors remain stronger than flexors
• Defect in the system cause UMN signs

26
Q

spinothalamic pathway

A
  • Fast pain – nociceptors, temperature, crude touch
  • Anterolateral
  • Neuronal axons enter via dorsal root into dorsal spinal cord → ascend or descend 1-2 vertebral levels → via Lissauer’s tract → then synapse with 2˚ neurons at either substantia gelatinosa or nucleus proprius.
  • These 2˚ axons decussate via anterior white comissure to anterolateral spinal cord
  • Synapse with 3˚ neurons at thalamus, in ventral posterior nucleus.
27
Q

dorsal column - medial lemniscus pathway

A
  • Discriminative touch, proprioception, vibration
  • Rapid large myelinated fibres
  • Axons from lower body → most medial → gracile tract
  • Axons from upper body [T6 and up] → more lateral → cuneate tract
  • Synapse with neurons in the gracile and cuneate nuclei at the lvl of medulla oblongata.
  • 2˚ neurons cross-over to form in medial lemniscus
  • Neurons synapse in thalamus to ventral posterolateral nucleus (neck, trunk, limbs) and cenral posteromedial nucleus (head)
28
Q

spina bifida is what

A

the failure of the vertebral canal to close normally because of a defect in vertebral development

29
Q

spina bifida: associated developmental defects

A

efective development of the spinal cord, brain stem, cerebrum, or cerebellum.

30
Q

types of spina bifida

A

spina bifida occulta and spina bifida with meningocele or meningomyeloele

31
Q

what is spina bifida occulta

A

simple defect in the closure of the vertebra

32
Q

what is spina bifida with meningocele or meningomyelocele

A

ac-like protrusions of the overlying meninges and skin that may contain portions of the spinal cord or nerve roots.

33
Q

what is Meningocele

A

herniation of the meningeal membranes through the vertebral defect. It usually causes a soft, cystic, translucent tumor to appear low in the midline of the back.

34
Q

what is meningomyelocele

A

nerve roots and the spinal cord protrude through the vertebral defect and usually adhere to the inner wall of the meningeal sac.

If the meningomyelocele is high in the vertebral column, the clinical picture may resemble that of complete or incomplete transection of the cord.

35
Q

associated abnormal signs with spina bifida (occulta)

A

fat deposits, hypertrichosis (excessive hair) over the affected area, and dimpling of the overlying skin. Symptoms may be caused by intraspinal lipomas, adhesions, bony spicules, or maldevelopment of the spinal cord.

36
Q

what is cauda equina syndrome?

A

a serious neurologic condition in which damage to the cauda equina causes acute loss of function of the lumbar plexus, (nerve roots) of the spinal canal below the termination (conus medullaris) of the spinal cord. CES is a lower motor neuron lesion.

37
Q

clinical feeatures of cauda equina syndrom

A

Signs of LMN lesions affecting both lower limbs
Acute urinary retention
Lower back pain
Perianal numbeness

Lax anal tone

38
Q

what is the pathology in cauda equina syndrome

A

Lumbosacral nerve roots that form cauda equina are compressed (usually centrally prolapsing intervertebral disc) → Lower motor neuropathy affecting bladder + bowel sphincters + lower limbs.

39
Q

treatment for someone presenting with cauda equina syndrome?

A

urgent neurosurgery opinion + MRI

40
Q

motor neuron disease is what?

A

a progressive condition causing weakness and eventually death (respiratory failure or aspiration)

41
Q

incidence of MND

A

2/100 000 50-70y/o

42
Q

pathology in MND

A

predominantly affects upper and lower motor neurones in the spinal cord, cranial nerve nuclei and cortex. Other neuronal systems may also be affected. 40% have frontotemporal dementia

43
Q

aetiology of MND

A

Usually sporadic, no known cause.

44
Q

pathological hallmarks of MND

A

ubiquinated cytoplasmic inclusions containing the ARNA processing proteins TDP-43 and FUS in axons – protein aggregations. Sensory system is not involved → no sx such as tingling, pain or numbness.

45
Q

diagnostic tests for MND?

A

there are none, but Ixs help exclude other disorders

46
Q

important differential for MND

A

cervical spondylosis causing radiculopathy with myelopathy (UMN and LMN signs)

47
Q

types of MND

A

ALS (amyothropic lateral sclerosis)
PMA (progressive muscular atrophy)
PLS (primary lateral sclerosis)
Progressive bulbar palsy

48
Q

PMA (progressive muscular atrophy) features

A
  • Flaccid weakness as only LMNs affected
  • Fasciculations and wasting
  • Decreased or absent reflexes
  • Plantars going down
49
Q

ALS features

A

amyotrophic lateral sclerosis
• Both UMN and LMNs affected simultaneously, so maybe flaccid or spastic
o Progressive focal muscle wasting with muscle fasciculations due to spontaneous firing from surviving branching axons
• Begins in one limb, gradually spreads further
• Weakness throughout, degree of weakness depends on the number of muscles affected and distribution of motor neuron loss
• Reflexes usually exaggerated (UMN and LMN signs), + spasticity
• Ankle clonus elicited
• Bilateral extensor plantar responses
• Sensation unaffected throughout
• Involvement of lower cranial nerves causes a pseudobulbar palsy

50
Q

PLS

A 
priamry alteral sclerosis
•	Rare
•	UMN signs only
•	Usually begins in lower limbs – spastic gait
•	Exaggerated reflexes
51
Q

progressive bulbar palsy

A

• 20%
• Only lower CN affected (IX,X,XII)
Donald duck-nasal speech
• Weaknes of palatal muscles – swallowing difficulties.
• Dysarthria, dysphagia, ansal regurgitation
• Fasciculated tongue with slow stiff movements

52
Q

CSF in guillain-barre syndrome

A

protein level in CSF elevated but without pleocytosis

53
Q

which neurones GBS affects predominantly?

A

Lower MOTOR neurones

NOP (24 decks)

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