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Year 4 - Neuro and Special Senses > Neurologu > Flashcards

Neurologu Flashcards

1
Q

How do you perform a LP?

A
  • With the patient standing, mark out L4 by joining a line between the highest points of the iliac crests.
  • Palpate above for L3 and below for L5.
  • The insertion site can be marked out either between L3/4 or L4/5 depending on the patient’s anatomical features.
  • Position the patient lying on their side in a fetal position: ask the patient to flex forwards whilst bringing their knees up towards their chest.

The needle passes through the following layers before it reaches the subarachnoid space:

  1. Skin
  2. Subcutaneous fat
  3. Supraspinous ligament
  4. Interspinous ligament
  5. Ligamentum flavum
  6. Dura mater
  7. Subdural space
  8. Arachnoid mater

As the needle passes through the three defined ligaments, three ‘pops’ (sudden reductions in resistance) will normally be felt. After the third ‘pop’ (ligamentum flavum) CSF should flow

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2
Q

What are some of the signs of UMN? Where is the damage?

A
  • Causes: damage to motor pathways (corticospinal tracts) anywhere from motor nerve cells in the pre-central gyrus of the frontal cortex, through the internal capsule, brainstem, cord to synapse anterior horn cells in the cort
  • Affects muscle groups (not individual muscles)
  • Sx
    • Weakness: typically pyrimadal
    • Hypertonia
    • Spasticity: in stronger muscles (e.g. arm flexors and less extensors)
      • Increased tone – velocity-dependent and non-uniform (rigidity – increased tone is not velocity dependents but constant through passive movement)
    • Hyperreflexia: reflexes are brisk
      • Plantars are upgoing – babinskis
      • Clonus – rapidly dorsiflexing foot
      • Hoffmans reflex – brief flexion if thumb and index finger in pincer movement
    • Clonus
    • Brisk tendon reflexes
    • Extensor plantar
  • UMN can mimic LMN lesions in the first few hours before the spasticity and hyperreflexia develop
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3
Q

What are some of the signs of LMN and where is the lesion?

A
  • Cause: damage anywhere from the anterior horn cells, nerve roots, peripheral nerves, plexi
  • Wasting:
  • Fasciculations: spontaneously involuntary twitching. Caused by upregulation of NAChR to compensate for denervation
  • Arreflexia; reduced tendon reflexes
  • Flexor plantars
  • Hypotonia
  • Weaknesses from primary muscle disease – symmetrical loss, reflexes re lost lar than in neuropathies and there is no SENSORY loss
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4
Q

What pathways are involved in LMN and UMN?

What is controlled by the DC and spinothalmic tracts

A
  • Motor Pathway: corona radiate -> internal capsule -> cerebral peduncles -> decussates at medullary pyramid -> lateral corticospinal tract -> anterior horn
  • DC – vibration, proprioception, 2 point dis,, fine touch - IPSILATERAL
  • Spinothalmic – temperature, pain, crude touch - CONTRALATERAL
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5
Q

What are some of the characteristic gait abnormalities seen and what do they signify?

A
  • Hemiplegic gait - abduction and circumduction of the affected limb in patients with UMN lesion affecting the leg – pyridimal contralateral
  • Spastic gait - scissoring gait found in spastic paraplegia
  • Steppage gait – in patients with footdrop the high stepping gait lifts the foot to avoid catching the toes. Can be bilateral.
  • Ataxic gait - road based, uncoordinated, unsteady gait characteristic of cerebellar syndromes or where there is loss of proprioception (ipsilateral)
  • Parkinsonian gait – shuffling, tremor
  • Romberg is a test of proprioception (DC)
  • Stroke: get people to put their arms out and see if they drift
  • Foot drop: LMN. Feet flop when they lift the leg.
  • Tandem walking – get them to narrow the base to see if they can walk on an even narrower gait.
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6
Q

What signs and symptoms are seen in cerebellar syndromes?

A
  • Gait – broad based ataxic gait – heel to toe or tandem walking
  • Nystagmus – hold patients gaze out to the side at a few seconds at a time
  • Speech – scanning
  • Dysarthria
  • Limb ataxia
  • Dysdiadokokinseia
  • Finger nose testing – pass point
  • Heel shin testing
  • Distribution – both legs, general cerebellar problem
  • Tone – reduced
  • Reflexes- pendular
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7
Q

What are some of the signs of movement disorders?

A
  • Hyperkinetic – with involuntary additional movement
  • Tremor.
  • Chorea. (athetosis.)
  • Dystonia.
  • Ballism. (Hemiballismus)
  • Myoclonus.
  • Hypokinetic – stiffness and slowness – e.g. Parkinson
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8
Q

What are some of the signs of

A
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9
Q

Where are expressive and receptive aphasia be localised to?

A
  • Broca’s: Expressive aphasia: Left posterior inferior frontal gyrus
  • Wernicke’s: Receptive aphasia: Posterior part of the superior temporal gyrus
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10
Q

How is a TIA managed?

A

Give aspirin 300 mg immediately

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11
Q

What are the different regional stroke symptoms that you get?

A
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12
Q

What are the symptoms of cerebellar stroke?

A
  • Headache, nausea, vomiting (sudden or progressive)
  • Dizziness or true vertigo (30%)
  • Visual disturbance (diplopia, blurred vision, oscillopsia)
  • Gait/limb ataxia
  • Speech disturbance (dysarthria or dysphonia)
  • Loss of consciousness (transient or comatose)
  • Obstructive hydrocephalus
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13
Q

How does a brain stem stroke present?

A
  • Rarely presents with an isolated symptom
  • Usually a combination of cranial nerve abnormalities, and crossed motor/sensory findings such as:

Signs

  • Double vision
  • Facial numbness and/or weakness
  • Slurred speech
  • Difficulty swallowing
  • Ataxia
  • Vertigo
  • Nausea and vomiting
  • Hoarseness
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14
Q

What are the 5 stages of migraine?

A
  • Premonitory or prodromal stage (can begin 3 days before the headache)
  • Aura (lasting up to 60 minutes)
  • Headache stage (lasts 4-72 hours)
  • Resolution stage (the headache can fade away or be relieved completely by vomiting or sleeping
  • Postdromal or recovery phase
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15
Q

What is the diagnostic criteria for migraines?

A
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16
Q

How are migraines managed?

A

Conservative: Non medication treatment: Hydration, Rest, Avoid trigger, Weight loss and Exercise; Cold and hot compress, massage, ‘4-head’

Acute: Simple analgesia:

  • 1st: Regular Paracetamol and ibuprofen
  • 2nd: Naproxen, Aspirin 900 mg
  • Sumatriptan, Antiemetic

Prophylactic:

  • Conservative: acupuncture, supplementation with vitamin B2 (riboflavin) severity.
  • Propranolol
  • Topiramate (SE: teratogenic)
  • Amitriptyline
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17
Q

How do you manage migraine specifically triggered around menstruation?

A

Prophylaxis with NSAIDs (e.g. mefanamic acid) or triptans (frovatriptan or zolmitriptan)

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18
Q

How do cluster headaches present?

A
  • Pain typical occurs once or twice a day, each episode lasting 15 mins - 2 hours
  • Clusters typically last 4-12 weeks
  • Intense sharp, stabbing pain around one eye (recurrent attacks ‘always’ affect same side)
  • Autonomic sx: redness, lacrimation, lid swelling, nasal stuffiness, miosis and ptosis in a minority
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19
Q

How are cluster headaches mx’d?

A
  • Acute: 100% oxygen, subcutaneous triptan (75% response rate within 15 minutes)
  • Prophylaxis: verapamil. There is also some evidence to support a tapering dose of prednisolone
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20
Q
A
21
Q

What are polyneuropathies?

A
  • Motor and/or sensory disorder of multiple peripheral or cranial nerves: usually symmetrical, widespread, and often worse distally (‘glove and stocking’ distribution).
  • They can be classified by: chronicity, function (sensory, motor, autonomic, mixed), or pathology (demyelination, axonal degeneration, or both).
22
Q

What is a sensory neuropathy?

A
  • Numbness; pins and needles, paraesthesiae; affects ‘glove and stocking’ distribution.
  • Difficulty handling small objects such as buttons.
  • Signs of trauma (eg finger burns) or joint deformation may indicate sensory loss.
  • Diabetic and alcoholic neuropathies are typically painful.
23
Q

What is motor neuropathy?

A
  • (Eg Guillain–Barré syndrome, lead poisoning, Charcot–Marie–Tooth syndrome.)
  • Often progressive (may be rapid); weak or clumsy hands; difficulty in walking (falls, stumbling); difficulty in breathing (↓vital capacity).
  • Signs: LMN lesion: wasting and weakness most marked in the distal muscles of hands and feet (foot or wrist drop). Hyporeflexia.
24
Q

What happens in cervical spondylosis?

A

Degeneration of the annulus fibrosus (the tough coating of the intervertebral discs) and osteophyte formation on the adjacent vertebra leads to narrowing of the spinal canal and intervertebral foramina.

25
Q

How does cervical sponylosis present?

A
  • Presentation: Neck stiffness (but common in anyone >50yrs old), crepitus on moving neck, stabbing or dull arm pain (brachialgia), forearm/wrist pain.
  • Signs: Limited, painful neck movement ± crepitus (examine gently). Neck flexion may produce tingling down the spine (Lhermitte’s sign).
26
Q

How does root compression (radiculopathy) present?

A
  • Pain/‘electrical’ sensations in arms or fingers at the level of the, with numbness, dull reflexes, LMN weakness, and eventual wasting of muscles innervated by the affected root.
  • NB: UMN signs below level of the affected root suggests cord compression.
27
Q

What are some of the features of cord compression?

A
  • Progressive symptoms (eg ↑weak, clumsy hands; gait disturbance)
  • UMN leg signs (spastic weakness, ↑plantars)
  • LMN arm signs (wasting, hyporeflexia); incontinence, hesitancy, and urgency are late features.
28
Q

How is spondylosis managed?

A
  • Medical: analgesia and encourage gentle activity.
  • Cervical collars
  • If no improvement in 4–6 weeks then MRI and consider neurosurgical referral for: interlaminar cervical epidural injections, transforaminal injections or surgical decompression
29
Q

What is MG?

A
  • Autoimmune condition that causes muscle weakness that gets progressively worse with activity and improves with rest.
  • Affects men and women at different ages. Women < 40 and man over the age of 60.
  • Strong link with thymoma (tumours of the thymus gland)
  • Autoimmune condition caused by AchR -Abs at the MNJ: these bind to the postsynaptic neuromuscular junction receptors.
  • This blocks the receptor and prevents the acetylcholine from being able to stimulate the receptor and trigger muscle contraction.
30
Q

What are the specific ABs for MG?

A
  • AchR-Abs (85%)
  • Remaining 15%
    • Muscle-specific kinase (MuSK)
    • LRP4: antibodies against low-density lipoprotein receptor-related protein
31
Q

How does MG present?

A
  • Weakness that gets worse with muscle use and improves with rest
  • Sx minimal in the morning and worst at the end of the day
  • Typically affect proximal muscles weakness and small muscles of H+N
    • Diplopia
    • Ptosis
    • Weakness in facial movements
    • Dysphagia
    • Fatigue in the jaw when chewing
    • Slurred speech
    • Dysphonia (rare)
    • Myasthenic snarl on smiling
32
Q

What signs should you look for when examining MG?

A
  • Repeated blinking will exacerbate ptosis
  • Prolonged upward gazing will exacerbate diplopia on further eye movement testing
  • Repeated abduction of one arm 20 times will result in unilateral weakness when comparing both sides
33
Q

What Ix are used for MG?

A
  • Bloods: CK normal
    • Antibodies
      • Acetylcholine receptor (ACh-R) antibodies (85% of patients)
      • Muscle-specific kinase (MuSK) antibodies (10% of patients)
      • LRP4 (low-density lipoprotein receptor-related protein 4) antibodies (less than 5%)
  • A CT or MRI thorax: thymoma.
  • Specialist:
    • Edrophonium test: give IV dose of edrophonium (neostigmine) – this blocks cholinesterase inhibitors which breakdown Ach causing it to increase at NMJ -> symptomatic release -> Diagnosis of MG
    • Single fibre electromyography
34
Q

How is MG mx’d?

A

Medical

  • Reversible acetylcholinesterase inhibitors (1st:pyridostigmine or neostigmine) – increased Ach at NMJ
  • Immunosuppression (e.g. 1st: prednisolone or 2nd: azathioprine)
  • Monoclonal antibodies: Rituximab is recommended by NICE
  • Surgery: Thymectomy can improve symptoms even in patients without a thymoma
35
Q

What is myasthenic crisis? How is it mx’d?

A
  • Causes an acute worsening of symptoms, often triggered by another illness such as RTI
  • Can lead to respiratory failure (due to weakness in the muscle of respiration)
  • Mx
    • IV immunoglobulins
    • Plasma exchange.
    • Surgery: NIV with BiPAP or full I+V
36
Q

What is GBS and who does it affect?

A
  • “Acute paralytic polyneuropathy” that affects the peripheral nervous system – peripheral neuropathy
  • Post-infectious: campylobacter jejuni, CMV, EBV
  • Rapidly progressive and potentially fatal
  • Commonest western acute flaccid paralysis
  • Bimodal peak – commonest in elderly
37
Q

What is the pathophysiology of GBS?

A
  • Frequently preceded by infection, trauma, surgery, vaccination, pregnancy or other immune system stimulation
  • Thought to occur due to a process called molecular mimicry. T
    • The B cells of the immune system create antibodies against the antigens on the pathogen that causes the preceding infection.
    • These antibodies also match proteins on the nerve cells.
    • They may target proteins on the myelin sheath of the motor nerve cell or the nerve axon.
38
Q

How does GBS present? (signs + sx)

A
  • Usually develop 1 to 3 weeks after URTI or GI infection
  • Often complain backache: central back pain – start of inflammation
  • Pain in the form of muscles cramps or hyperesthesias (worse at night).
  • Symptoms peak by 4 weeks – can be recurrent
  • Brief plateau – recover over weeks to months
  • Signs: hyporeflexia, symetrical ascending weakness, peripheral loss of sensation
39
Q

What are some of the features of diagnostic criteria for GBS?

A

Required features:

  • Progressive weakness in both arms and legs – bilateral – symmetrical
  • Areflexia (or hyporeflexia)

Features supportive of diagnosis

  • Progression of symptoms over days to 4 weeks
  • Relatively symmetric
  • Mild sensory signs or symptoms
  • CN involvement, especially bilateral facial weakness
  • Recovery begins 2-4 weeks after progression ceases
  • Autonomic dysfunction
  • Absence of fever at onset
  • Typical CSF and EMG/NCS features
40
Q

How is GBS Ix’d

A
  • EMG/ nerve conduction studies
  • LP for CSF - ↑protein, N/ mild including lymphocytes
  • Campylobacter serology if GI upset
    • AMAN – anti GM1, C Jejuni
    • MF – anti GQ1B
    • Anti-ganglioside antibodies
  • Stool cultures
  • Throat swab
41
Q

What are some common complications of GBS?

A
  • Autonomic dysfunction
  • Cardiac arrythmias - sinus tachy
  • Postural hypotension
  • Hypertension
  • Urinary retention
  • Ileus
  • Respiratory failure (T2)
42
Q

How is GBS managed?

A
  • IV immunoglobin. CI: MI
  • Plasmapheresis - within the first 2 weeks of onset
  • VTE prophylaxis (Leading cause of death is PE)
  • Therapeutic management: general, bedside spirometry, ventilatory support, ECG +/- cardiac monitoring, nutritional support +NGT, DVT, urinary cathetar, laxatives, pain control
43
Q

What is MND?

A
  • It is progressive, ultimately fatal condition where the motor neurones stop functioning.
  • No effect on the sensory neurones and patients should not experience any sensory symptoms or sphincter disturbance
  • Can be inherited: autosomal dominant (10% of cases)
44
Q
A
45
Q

What are the different types of AMD and what are their features?

A

Most common: Amylotrophic lateral sclerosis: UMN (legs) + LMN signs (arms)

  1. 2nd most common: Progressive bulbar palsy: (UMN) – WORST PROGNOSIS: affects cranial nerves ix–xii and so it affects primarily the muscles of talking and swallowing: flaccid, fasciculating tongue; jaw jerk is normal or absent, speech is quiet, hoarse, or nasal
  2. Progressive muscular atrophy: LMN signs only (distal before proximal)
  3. Primary lateral sclerosis: UMN signs, marked spastic leg weakness and pseudobulbar palsy. No cognitive decline.
46
Q

How does MND present?

A
  • Insidious, progressive weakness of the muscles throughout the body affecting the limbs, trunk, face and speech. The weakness is often first noticed in the upper limbs.
  • Increased fatigue when exercising.
  • Clumsiness, dropping things more often or tripping over.
  • Dysarthria: They can develop slurred speech
  • Tumbling spastic gait, foot-drop ± proximal myopathy, weak grip (door-handles don’t turn) and shoulder abduction (hair-washing is hard), or aspiration pneumonia
  • Fronto temporal dementia
47
Q

What does MND not affect?

A
  • Doesn’t affect external ocular muscles
  • No cerebellar signs
  • Abdominal reflexes are usually preserved and sphincter dysfunction if present is a late feature
  • No sensory loss
48
Q

How is MND mx’d?

A
  • Riluzole can slow the progression of the disease and extend survival by a few months in ALS.
  • NIV
  • Symptomatic management
    • Excess saliva: glycopyrronium bromide + Botulinum toxin A
    • Dysphagia: Blend food. Gastrostomy
    • Spasticity: Exercise, orthotics., baclofen
    • End-of-life care: Palliative care team. Consider opioids to relieve breathlessness and discuss NIV
49
Q

What is the prognosis if MND + complications?

A
  • Prognosis: poor: <3 years onset.
  • Respiratory failure or pneumonia -> death

Year 4 - Neuro and Special Senses (8 decks)

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