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Neuromuscular disorders Flashcards

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1
Q

Peripheral nerves

A

12 pairs of cranial nerves and 36 pairs of spinal nerves

Contain both motor and sensory axons

Limbs supplied by nerves from brachial or lumbosacral plexi

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2
Q

Neuromuscular juntion

A

Axon terminal, a synaptic cleft, and the endplate region of skeletal muscle

Junction is a transducer (electrical to chemical)

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3
Q

Clinical signs of muscle/nerve/synapse dysfunction

A

Generailsed weakness

Split into neuropathies, myopathies, and juctionopathies

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4
Q

Clinical signs of neuropathies

A

LMN disease

Usually severe impairment of motor function

Gait: Flaccid paresis or paralysis

Postural reaction: deficits

Spinal reflexes: Reduced/absent

Muscle tone: decreased to absent

Muscle mass: neurogenic muscle atrophy

Sensation: Decreased (hypoesthesia) to absent (anaesthesia). Paraesthesia, auto-mutilation

Cranial nerve deficits: V, VII, IX, X/XI, dysphagia, dysphonia, regurgitation due to megaoesophagus

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5
Q

Clinical signs of myopathies

A

Ventroflexion of the neck - especially in cats

Gait: generalised weakness, exercise intolerance, stiff and stilted

Postural reactions: usually normal

Spinal reflexes: usually normal

Muscle tone: usually normal

Muscle mass: muscle atrophy

Sensation: Usually unaltered, but can have muscle pain on palpation

Cranial nerve deficits: Usually unaltered but may be altered by involvement of masticatory muscles or impairment of swallowing

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6
Q

Neuromuscular diagnostic investigation (NM)

A

Haematology
Serum biochem (creatinine kinase and electrolytes)
Urinalysis (glucosuria, myoglobinuria)

Chest x-rays (megaoesophagus, aspiration pneumonia)

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7
Q

Peripheral nerve disorders causing generalised weakness

A

Idiopathic polyradiculoneuritis

Protozoal neuritis-myositis

Diabetes

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8
Q

Muscle diseases causing generalised weakness

A

Protozoal neuritis-myositis

Polymyositis

Hypokalaemia

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9
Q

Neuromuscular diseases causing generalised weakness

A

Myasthenia gravis

Botulism

Organophosphate and carbamates

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10
Q

Infectious causes of nerve/muscle ‘generalised weakness’

A

Protozoal polyradiculoneuritis-myositis

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11
Q

Inflammatory causes of nerve generalised weakness

A

Idiopathic polyradiculoneuritis

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12
Q

Inflammatory causes of muscle generalised weakness

A

Idiopathic polymyositis

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13
Q

Inflammatory causes of NM junction generalised weakness

A

Myasthenia gravis

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14
Q

Indiopathic causes of muscle generalised weakness

A

Exercise induced rhabdomyolysis

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15
Q

Toxic causes of nerve generalised weakness

A

Vincristine

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16
Q

Toxic causes of Muscle generalised weakness

A

Toxic rhabdomyolysis

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17
Q

Toxic causes of muscle generalised weakness

A

Botulism, organophosphates/carbamates, aminoglycosides

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18
Q

Metabolic causes of nerve generalised weakness

A

Diabetes mellitus
Hypothyroidism

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19
Q

Metabolic causes of muscle generalised weakness

A

Cushing’s myopathy
Hypothyroidism
Hypoadrenocorticism
Hypokalaemic myopathy

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20
Q

Neoplastic causes of nerve generalised weakness

A

Paraneoplastic: insulinoma

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21
Q

Neoplastic causes of muscle generalised weakness

A

Paraneoplastic: lymphoma

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22
Q

Neoplastic causes of NM junciton generalised weakness

A

Paraneoplastic

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23
Q

Degenerative causes of nerve generalised weakness

A

Inherited neuropathies

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24
Q

Degenerative causes of muscle generalised weakness

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A

Inherited myopathies

25
Degenerative causes of NM junction generalised weakness
Myasthenia congenita
26
Pathogenesis of idiopathic polyradiculoneuritis
Signs caused by immunemediated attach to the axons and myelin sheaths at level of ventral nerve roots
27
Epidemiology of idiopathic polyradiculoneuritis
Most common peripheral neuropathy
28
Clinical signs of of idiopathic polyradiculoneuritis
Start acutely in the pelvic limbs Rapidly progress to LMN tetraparesis or tetraplegia
29
DIfferential diagnosis of idiopathic polyradiculoneuritis
Looks very similar to Botulism, but in botulism the cranial nerve deficits are more prominent
30
Diagnosis of idiopathic polyradiculoneuritis
Electromyography reveals denervation potentials Nerve conduction velocities are reduced CSF can show an increase in mononuclear cells. Bloods (serology neospora exclusion)
31
Prognosis of idiopathic polyradiculoneuritis
Outcome is good - recover over a period of 3-6 weeks
32
Treatment of idiopathic polyradiculoneuritis
Supportive care and rehabilitation Corticosteroid administration is not beneficial Monitor pulmonary function
33
Pathogenesis of myasthenia gravis
Failure of NM transmission due to reduction in number of functional nicotinic actylcholine receptors An immune-mediated disease caused by an over-production of antibodies directed against acetylcholine receptors
34
Epidemiology of myasthenia gravis
Relatively common in dogs Relative rare in cats Usually occurs spontaneously Can be associated with thymoma or other neoplastic/immunemediated diseases
35
Clinical signs of myasthenia gravis
Focal: facial, oesophageal, laryngeal, and pharyngeal weakness, resulting in regurgitation and dysphagia Generalised: exercise intolerance, regurgitation, stiff gait with short strides Acute fulminant form of generalised: very rapid onset or paralysis and regurgitation - rare
36
Diagnosis of myasthenia gravis
Resolution of muscle weakness following IV injection of edrophonium chloride Repetitive nerve stimulation- decremention of the action potential Serum sample: ACh antibodies Chest x-ray for cranial mediastinal mass
37
Prognosis of myasthenia gravis
Good Clinical remission is 6 months Guarded if persistent megaoesophagus
38
Treatment of myasthenia gravis
ACh inhibitors - pyridostygmine - neostigmine in case of severe regurgitation Immunosuppressive therapy - steroids - controversial
39
Neuromuscular diseases causing 'focal weakness'
Aortic thromboembolism Masticatory myositis (muscle) Brachial plexus avulsion Sciatic nerve injury Nerve sheath tumour
40
Pathogenesis of aortic thrombosis
Obstruction of aortic or iliac arteries Common underlying cause: hypertrophic cardiomyopathy Restriction of blood flow by embolus causes ischaemia to the sciatic nerve and muscles of the pelvic limbs
41
Epidemiology of aortic thrombosis
Most commonly seen in cats
42
Clinical signs of aortic thrombosis
Acute onset of pelvic limb paresis/plegia, loss of pelvic limb nociception distally, Weak or absent femoral pulse Cold limbs Cyanotic nail beds Very painful Signs of heart failure may be present
43
Diagnosis of aortic thrombosis
Based on clinical signs Marked elevated serum CK present in first 1-2 days Chest x-rays and echocardiography - evidence of cardiac disease
44
Prognosis of aortic thrombosis
Long term prognosis poor - association with heart disease Worth treating if pain can be controlled
45
Treatment of aortic thrombosis
Management of cardiac disease Low dose aspirin to prevent further blood clots - controversial Pain relief is mandatory
46
Pathogenesis of (malignant) peripheral nerve sheath tumours
Aggressive biological behaviour Most commonly affects the caudal cervical (C6-C8) and cranial thoracic (T1-T2) Spread slowly May invade vertebral canal causing spinal cord compression Highly invasive locally but rarely metastasize
47
Epidemiology of (malignant) peripheral nerve sheath tumours
Brachial plexus tumours are seen in adult, older dogs. Cats will rather have a lymphoma of the brachial plexi
48
Clinical signs of (malignant) peripheral nerve sheath tumours
Slowly progressive thoracic lameness, paresis and muscle atrophy Pain on palpation of the axillary region Axillary mass may be palpable Ipsilateral partial or complete Horner's syndrome, and ipsilateral absent cutaneous trunci reflex
49
Diagnosis of (malignant) peripheral nerve sheath tumours
Diagnosis by exclusion of orthopaedic disease and radiographs of thoracic limbs. Electromyogram shows abnormal and spotnaeous muscle activity Chest x-rays and abdominal ultrasound performed to metastatic disease MRI of brachial plexus or peripheral nerves can visualise the nerve root tumour
50
Prognosis of (malignant) peripheral nerve sheath tumours
Poor with high recurrence rate after surgery (amputation)
51
Treatment of (malignant) peripheral nerve sheath tumours
Local excision is rarely possible; usually leg amputation with or without spinal decompression is needed
52
Pathogenesis of brachial plexus trauma
Usually caused by a road traffic accident or fall from height - abduction and caudal displacement of thoracic limbs Site of avulsion is usually intradural
53
Epidemiology of (malignant) peripheral nerve sheath tumours
Most common cause of acute thoracic limb monoparesis/plegia in small animals
54
Clinical signs of (malignant) peripheral nerve sheath tumours
Peracute onset of monoparesis/plegia following traumatic incident Avulsions Ipsilateral partial Horner's syndrome and/or loss of cutaneous trunci reflex
55
Three types of avulsion
Cranial avulsions (C6-7) - rare, few clinical signs Caudal (C8-T2) or Complete (C6-T2) - more common - more severe clinical signs - paralysis of brachial triceps
56
Diagnosis of (malignant) peripheral nerve sheath tumours
Acute history of a traumatic incident Electromyogram allows detection of spontaneous electrical activity in denervated muscles 7-10 days after injury
57
Prognosis of (malignant) peripheral nerve sheath tumours
Most cats still have pain sensation on presentation, compared to dogs Prognosis is good if deep pain sensation is present If deep pain absent, prognosis will depend on the severity of the axonal injury
58
Treatment of (malignant) peripheral nerve sheath tumours
No routinely effective treatment Amputation of limb may be needed but wait 2-3 months to see if recovery occurs

SA Neurology (11 decks)

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