Neurology Module 3 Flashcards

1
Q

What should always be assessed when localising lesions?

A
  1. Mentation
  2. Gait
  3. Proprioception
  4. Spinal reflexes
  5. Pain
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2
Q

What is the shiff-sherington posture?

A

Hyperextension of TL and paralysis of PLs
- Interference with border cells
- Inhibitoru meurons in cranial lumbar spinal cord that inhibit TL extensor muscles
T3-L3
Not a prognostic factor

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3
Q

What are the thoracic limb reflexes?

A
  1. Withdrawal reflex - most reliable - put cats on their back
  2. Extensor carpi radialis reflex
  3. Biceps/triceps
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4
Q

What are the pelvic limb reflexes?

A

Withdrawal reflexes
Patellar reflex
cranial tibial reflex
gastronemius
perineal S1-S3 pudendal n

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5
Q

What is the cutaneous trunci reflex?

A

Pinprick stimulus applied to the skin at L5 and subsequently more cranial - the reflex spread through the whole arc so if normal at the bottom then no need to continue
If response is absent then two vertebrae cranially is the cause (t3-L3 lesion)

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6
Q

Which limbs will be affected with lesions at, C1-C5, C6-T2, T3-L3, L4-S1

A

C1-C5 - All 4 limbs - normal to increased reflexes
C6-T2 - All 4 limbs - reduced TL, normal to increased
T3-L3 - Peripheral limbs - TL normal, HL increased to normal
L4-S1 - Peripheral limbs - TL normal, HL reduced
Polyneuropathies: reduced all limbs

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7
Q

CS of neuromuscular disease with: MN, SN,

A

Motor neuron disease - flaccid paralysis, decreased tone and atrophy
Sensory neuron disease - postural deficits, decreased sensation +/- paraaesthesia (self mutilation)
Can affect one: trigeminal, facial, radial
Can affect a group: brachial plexus avulsion, cranial neuropathy, ischaemic neuromyopathy (saddle)

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8
Q

What are examples of junctionopathies?

A

Presynaptic - botulism
Postsynaptic - MG - weakness worsens with exercise
Enzymatic - organophosphates

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9
Q

How do myopathies present?

A

Generalised weakness and or exercise intolerance
- neck ventroflexion, stiff-stilted gait
No proprioceptive or spinal reflexes
Variable muscle tone and bulk
Can be generalised: inherited/degen, inflam/infection, metabolic (Na, K, Ca)
Focal - masticatory myositis

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10
Q

Steroid responsive meningitis: CS, DDX, Dx, Tx

A

Aseptic, non-suppurative meningitis - 6-18mths
CS: spinal pain (neck), pyrexia, lethargy, stiff gait, sometimes IMPA concurrent - acute and chronic form
Dx: CSF - neutrophilic if acute, mononuclear pleocytosis chronic
+/- diagnostic imaging CT/MRI
+/- serum IgA in CSF

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11
Q

Discospondylitis: CS, Dx, Tx

A

CS: Severe pain, middle aged to large breed dogs, pyrexia, anorexia
Dx: images take 2-4 weeks to show changes - MRI/CT, X-rays - narrowing IVd, roughening of endplates, proliferation of adjacent bone
Bacteriology of urine/blood
Tx: abs for 8-12weeks, gaba, NSAIDs

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12
Q

What is empyema and how is it treated?

A

Pus within the epidural space
CS: pain, pyrexia, progressive myelopathy
Causes: epidural anaesthesia, spinal surgery, bite wounds, hematogenous spread, osteomyelitis extension
Tx: Decompression surgical + antibiotics

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13
Q

How do you determine instability with fractures of vertebrae?

A

Vertebrae split in to dorsal/middle/ventral
2 or more fractures in 2 or more compartments = surgery
If stable - splint and cage rest

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14
Q

Prognosis IVDD

A

1-5 grade
1 - no deficits/pain conservative 100% conservative
2. paresis, ambulatory 95% surgical
3. paresis non-amulatory 95% surgical
4. paralysis 95% surgical
5. no deep pain 50-60% if surgery in 36-48hrs, 5% if medically managed

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15
Q

What are the causes of lumbosacral disease?

A
  • Type 2 IVDD
  • Hyperthrophy of ligaments
  • Hypertrophy of synovia
  • foraminal stenosis
  • ventral subluxation of sacrum
  • sclerosis of vertebral endplates and articular processes

Pain management with surgical tx

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16
Q

What is the difference of an UMN bladder v. LMN bladder?

A

UMN: Lesions cranial to the sacral spinal cord that interrupt eff/aff pathways - impaired volumtary mictruition and distended difficult to express bladder

LMN: Lesions in sacral spinal cord, pudendal n, pelvis. Distended bladder and continually dribbling

17
Q

What is the diagnostic workup of a collapse?

A
  1. Haematology &Biochemistry: glucose, electrolytes, CK
  2. Urinalysis and culture
  3. Serology for infections : neospora, toxo
  4. Serology for IM disease: myasthenia gravis, type 2M antibody titre
  5. Endocrine: thryoid/adrenal
  6. Edrophonium or neogostimine test - MG
  7. Genetic testing: centronucleaur myopathy (lab) exercise induced collapse (lab), episodic collapse (CKCS)
  8. Imaging: chest rads/abdo u/s
  9. electrphysiology
  10. Muscle/nerve biopsy
18
Q

What is the most common neuropathy?

A

Acute polyradiculoneuritis
- inflammation of both peripheral roots and nerve roots
- thought to be aberrant immune response to infection - coonhound paralysis/vaccination
- Acute and progressive - starts in FL and progresses to HL
- resp failure possible - ventilator

19
Q

Botulism: CS, Dx, Tx

A

Ingestion of food or dead animals contaminated with endotoxin produced by bacteria - Clostridium botulinum spores
CS: acute and rapidly progressive, pelvic limbs affected over 2-3 days and then spreads to thoracic limbs leading to non-ambulatory tetraparesis, autonomic signs: urinary dysfunction, dilated pupils, megaoesophagus
Dx: C/S, toxin, electrophysiology
Tx: supportive care, antioxins and possible abs

20
Q

What are the types of myasthenia gravis?

A
  1. Focal form - 40% dysphagia, regurgitation
  2. Generalised form - exercise intolerance, possible megaoesophagus (pharyngeal, laryngeal dysfunction)
  3. Fulminant form - rapid progression of non-ambulatory tetraparesis + megaoesophagus
  4. Cats - 15% focal also associated with thymoma 25%
21
Q

What is the treatment for myasthenia gravis?

A

Pyridostigmine PO or neostigmine IM - cholinesterase inhibitors
immunosuppression
thymoma removal

22
Q

Tetanus: CS, Dx, Tx

A

Tetanus spores in an anaerobic environment (necrotic wound) converts to vegetative form that produces toxin) - peripheral neurons transfer tetanospasmine to CNS
CS: 4-12 days rigidity, hyperextension of limbs, trismus, dysphagia, risus sardonicus, elevated tail/ears, seizures, urinary/fecal retention, hypersensitivity
tx: identify and debride wound, antibiotic metronidazole (stops toxin production), anti toxin to neutralise toxin
ACP/BZP + pheno
methocarbamol - muscle relaxation
MgSO4 - helps with muscle relax
Supportive care

23
Q

Causes of infectious myositis?

A

neospora/toxoplasma
Neospora - ascending paralysis
dx: raised CK/AST, EMG, muscle biopsy, serology

24
Q

What breed does centronuclear myopathy affect?

A

Inherited disease, young 2mth-12mths Labs
generalised weakness, poor muscle conformation, absent patellar reflexes
DNA test available

25
Q

What the difference between myokymia and neuromyotonia?

A

Myokymia - muscle rippling
Neuromyotonia - abnormal muscle tone
persists through GA and sleep - motor axon and terminal hypersensitivity
JRT - with hereditary ataxia
CS: collapse, rigidity, recumbency, rhythmic undulating m. contractions
tx mexilitine

26
Q

What are sleep disorders commonly seen

A

Narcolepsy/Cataplexy (sudden loss of motor tone)
- disorder of sleep/wake control
- DNA test in dachsy/lab
- REM disorders - loss of inhibiton of LMN selectively

27
Q

What are ddx for acute spinal disease that are progressive?

A

Infectious/Inflammatory: MUO, Neo/Toxo, discospondylitis, FIP, FELV, SRMA, Empyema

Anomalous: AA sublux, canine chiari

Neoplasia

Degenerative disease: IVDD, CCS, LSDD

28
Q

What are ddx for acute spinal disease that are non-painful?

A

Anomalous: bony changes, vertebral anomalies
Neoplastic
Degenerative