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Neurology Flashcards

1
Q

Multiple Sclerosis

A

Wide range of clinical symptoms and signs:

  • Sensory, motor, cerebellar, cognitive
  • Optic neuritis
  • INO
  • Acute partial myelopathy
  • Lhermitte’s (electric shock sensation) and Uhthoff’s symptoms (elevated temperature impairs vision)
  • Exercise-induced symptoms
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2
Q

Types of Multiple Sclerosis

A

Relapsing Remitting (RRMS)

  • commonest type (>2/3 patients at onset)
  • recovery between acute relapse episodes
Primary Progressive (PPMS)
- progressive deterioration from disease onset without clear relapses and remissions.
Secondary Progressive (SPMS)
- relapses/remissions then progressive deterioration.
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3
Q

MS Lesion Characteristics

A

Characteristic appearance and distribution of lesions:

  • Periventricular, corpus callosum, centrum semiovale
  • Radiating out from corpus callosum = Dawson’s fingers
  • Brainstem, cerebellum
  • Hyperintense on T2
  • Hypointense on T1
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4
Q

Multiple Sclerosis Diagnosis

A

Clinical history and examination.
MRI.

Evoked potentials (EPs)

  • VEP = visual EP (optic neuritis)
  • SEP = somatosensory (limbs)
  • BAER = brainstem EP = auditory pathways

Central Motor Conduction Time (CMCT)

  • Motor pathways = corticospinal tracts to limbs
  • MEPS = motor evoked potentials
Lumbar Puncture (LP)
- oligoclonal bands +ve in CSF but NOT in serum, increased CSF IgG synthesis
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5
Q

Natalizumab

A

Alpha-4 integrin antagonist.
Selective adhesion molecule inhibitor.
MRI monitoring re. risk of PML
(Risk factors: JC virus positivity, prior immunosuppressive treatment, longer duration of Natalizumab treatment).

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6
Q

PML

A

Progressive multifocal leukoencephalopathy
Rapidly progressive demyelination in brain
Dementia, motor dysfunction, visual loss.
JC (polyoma virus) infection of oligodendrocytes.
Diagnosis JC virus in CSF via PCR.
MRI abnormal
Tx: immune reconstitution

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7
Q

Alemtuzumab

A

Humanised monoclonal Ab binds to CD52 (on B cells).

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8
Q

Fingolimod

A

Decreases the ability of lymphocytes to enter CNS by preventing the egress of lymphocytes from lymphatic tissues.
Reduces relapse rate and decreases new MRI lesions.
Potential cardiac SEs.

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9
Q

Neuromyelitis Optica (NMO)

A

a rare condition where the immune system damages the spinal cord and the nerves of the eyes (optic nerves).

Not typical MS. 90% recurrent events, may be severe, may be little improvement.
90% women
Aquaporin 4 NMO antibodies
Channelopathy, aquaporin 4 predominant water channel in CNS
Doesn’t respond to interferon or other MS therapies - treatment is immunosuppression (steroids or Rituximab)
Worse prognosis than MS

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10
Q

MOG Antibody Disease

A

MOG = Myelin Oligodendrocyte Glycoprotein disease
MS mimicker
ADEM presentation in children
Opticospinal (NMO type) in adolescents and adults -> optic neuritis and transverse myelitis.

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11
Q

INO

A 
Typical feature of MS
Due to lesion in MLF
Loss or slowed ADDuction
Horizontal nystagmus of ABDucting eye
Lesion in MLF on side of decreased ADDuction
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12
Q

Temporal patterns of peripheral nerve disease

A

Acute: GBS, vasculitis, porphyria, infectious, toxic/drug
Subacute: toxic, nutritional, malignancy, paraneoplastic, metabolic
Chronic: inherited

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13
Q

Associated Phenomena Peripheral Neuropathies

A 
Preceding infections or diarrhoea:
- GBS (Campylobacter jejuni)
Associated diseases:
- Diabetes, renal, hepatic failure, thyroid dysfunction
Medications:
- Vinca alkaloids, cis platinum, amiodarone
Toxins:
- Lead, arsenic, thallium
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14
Q

Hereditary Motor and Sensory Neuropathy

A

HMSN1 = demyelinating, HMSN2 = axonal

HMSN1 (CMT 1)

  • uniformly slowed nerve conduction velocities (<38m/s)
  • dispersion and conduction block are rarely seen in comparison to acquired demyelinating neuropathies
  • demyelination
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15
Q

Paraneoplastic Sensory Neuropathy

A

SCLC most commonly implicated
Sensory symptoms precede diagnosis of cancer by months
Pain and paraesthesiae - 1 limb, asymmetry, arms
Rapidly progressive (weeks)
All modalities of sensation affected

CSF: increased protein, pleocytosis, lymphocytes, OCBs positive, IgG ratio abnormal

NCS: decreased or absent SEPs and SNAPs, motor NCS and EMG may be normal

Antineuronal nuclear antibodies (ANNA) 1 = anti-Hu

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16
Q

Inclusion Body Myositis

A 
Usually >50 years
Commoner in men
Proximal and distal
Finger and wrist flexors
Quadriceps
Atrophy prominent
Dysphagia in one third
Poor response to steroids, immunoglobulin
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17
Q

Myasthenia Gravis

A

Symptoms: ptosis (not fixed, fatiguable), diplopia, limb weakness, neck weakness, SOB (emergency).
80% of MG has positive AChR AB, which are pathogenic, but levels correlate poorly with disease severity.
Association with hyperthyroidism, SLE, scleroderma and RA.

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18
Q

MuSK MG

A

20% have antibodies to muscle specific kinase
Thymus usually normal
HLA DR14-DQ5 association
Limb muscles often less affected
Progresses to severe facial and bulbar weakness, with atrophy of affected muscles
May require different treatment (Ritux)

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19
Q

MG Treatment

A

Acetyl-cholinesterase inhibitors: Pyridostigmine
Steroids
Steroid-sparing agents
Rituximab/Eculizumab

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20
Q

Myasthenic Crisis

A 
Severe enough to endanger life.
Diaphragm/intercostal muscle involvement.
ICU.
Treat infection if present.
Increase Prednisolone.
Plasma exchange or IVIG.
Thromboprophylaxis.
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21
Q

LEMS

A

50% paraneoplastic - mainly SCLC.
Also non-SCLC.
Other 50% autoimmune disorders.
HLA B8 DR3 association.
IgG antibodies against voltage-gated calcium channels.
Weakness usually worse in lower limbs (proximal), not usually fatiguable.
Bulbar weakness and diplopia typically less persistent and severe than in MG.
Distal symmetrical sensory neuropathy.
Autonomic neuropathy (dry mouth/eyes and impotence).
Reflexes depressed, but potentiate as does power.

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22
Q

Treatment of LEMS

A

3-4 Diaminopyridine (potassium channel blocker)
Immunosuppression (as for MG)
Treat malignancy if present

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23
Q

Neurophysiological Diagnosis of NMJD

A

In LEMS and MG, at low frequency (1-5 Hz) there is a decrement with repetitive motor nerve stimulation.

In LEMS but not MG, at high frequency (20-50Hz) repetitive stimulation there is an incremental response.

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24
Q

NMDAR Encephalitis

A

F4:M1
50% of females have ovarian teratoma
Psychiatric features followed by movement disorder, drowsiness and seizures.

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25
Q

LGI1 encephalitis

A

Older patients, 10% associated with breast, thymoma, thyroid cancers and lymphoma
Hyponatraemia, faciobrachial seizures, drowsiness and amnesia.
Diagnosis is often delayed.
MRI - high signal in median temporal lobes
Initial treatment with steroids

26
Q

What genes are associated with MND?

A

C9ORF - most common
Zn/Cu SOD1 - 20%
Fus - 5%

27
Q

Which APOE forms increase risk of AD?

A

E4

28
Q

Stiff-person Syndrome

A

Strong association with GAD antibodies at higher titres than in DM1.

29
Q

Levetiracetam MOA

A

Synaptic vesicle protein 2A inhibition of Ca2+ currents
No interactions with OCP/warfarin
95% renally excreted
Irritability, mood swings

30
Q

Perampanel

A

Glutaminergic AMPA antagonist.

Adjunctive for focal seizures.

31
Q

AED to avoid in women of childbearing age:

A
  1. Polytherapy
  2. Phenobarbitone
  3. Valproate
32
Q

AED and visual field loss

A

Vigabatrin (Sabril™) causes visual field constriction in around 30% of users.

33
Q

Meniere’s Disease

A

The clinical triad of Meniere disease are episodic vertigo, sensisorineural hearing loss and tinnitus.

34
Q

Friedrich’s ataxia

A

Almost all patients with Friedrich’s ataxia presents with limb ataxia. Early loss of position and vibration sense occurs, reflecting posterior column spinal cord dysfunction, as well as dorsal root and peripheral, primarily sensory, axonal neuropathy.

35
Q

A 30 year old man has a painful right eye. On examination, there is decreased visual acuity and a relative afferent pupillary defect of the right eye. What is the diagnosis?

A

Optic neuritis

36
Q

CLIPPERS

A

Chronic lymphocytic inflammation with pontine perivascular enhancement responsive to steroids (CLIPPERS) is an uncommon and only recently described disorder characterised by infiltration of the brain by inflammatory cells. It has a predilection for the pons, with fairly characteristic curvilinear regions of enhancement best seen on MRI. The disorder usually readily responds to immunosuppression with glucocorticosteroids. Patients typically present subacutely with a wide variety of signs and symptoms dominated by cranial nerve dysfunction,cerebellar signs and long tract signs.

37
Q

Gerstmann’s syndrome

A

agraphia, acalculia, finger agnosia, left right disorientation.

38
Q

Wallenberg’s syndrome

A

Wallenberg’s syndrome is also known as lateral medullary syndrome. It is due to occlusion of the posterior inferior cerebellar artery, and the features are as described in the question. Features commonly seen in Wallenberg syndrome: – Ipsilateral loss of facial pain and temperature(due to trigeminal spinal nucleus and tract involvement). – Contralateral loss of pain and temperature(due to damage to the spinothalamic tract). – Ipsilateral palatal, pharyngeal, and vocal cord paralysis with dysphagia and dysarthria (due to involvement of the nucleus ambiguus). – Ipsilateral Horner syndrome (due to affection of the descending sympathetic fibers). – Ipsilateral cerebellar signs and symptoms (due to involvement of the inferior cerebellar peduncle and cerebellum). – Vertigo, nausea, and vomiting (due to involvement of the vestibular nuclei).

39
Q

Which of the following mutation occurs in the Familial form of Amyotrophic Lateral Sclerosis(FALS)?

A

SOD1

40
Q

Riluzole MOA

A

Riluzole is a sodium channel blocker that inhibits glutamate release.May slow progression of disease marginally.

41
Q

Which of the following anti-epileptic drug may cause osteoporosis?

A

Phenytoin

42
Q

Painful third nerve palsy =

A

posterior communicating artery aneurysm

43
Q

Weber’s syndrome

A

Ipsilateral third nerve palsy with contralateral hemiplegia

44
Q

Which of the following AED will most likely cause Steven Johnson Syndrome?

A

Lamotrigine

45
Q

Differentials for foot drop

A

Is an injury to… Common peroneal nerve Sciatic nerve (loss or reduced ankle jerk) L5 radiculopathy.

46
Q

Medial medullary infarct

A

1) ipsilateral hypoglossal palsy, 2) contralateral hemiparesis, 3) contralateral lemniscal sensory loss.

47
Q

Hemiballismus

A

A rare movement disorder characterised by a large movement of an entire limb or limbs on one side of the body. It is often caused by focal lesions in the contralateral basal ganglia and subthalamic nucleus.

48
Q

Weber Syndrome

A

Weber syndrome, classically described as a midbrain stroke syndrome and superior alternating hemiplegia, involves oculomotor fascicles in the interpeduncular cisterns and cerebral peduncle, thereby causing ipsilateral third nerve palsy with contralateral hemiparesis. It most commonly results from the occlusion of a branch of the posterior cerebral artery.

49
Q

Horner Syndrome

A

Enophthalmos, miosis, ptosis and anhydrosis.

50
Q

S1 radiculopathy

A

S1 innervates the skin over the little toe and S1 radiculopathy is associated with loss of ankle jerk.
Decreased plantar and toe flexion.

51
Q

L5 radiculopathy

A

Associated with decreased foot dorsiflexion and toe extension with normal ankle jerk.

52
Q

Common peroneal nerve compression

A

Leads to foot drop with weakness on foot dorsiflexion and eversion. Can be seen with prolonged immobilisation such as following general anaesthesia or from casts. Reflexes are preserved.

53
Q

Sciatic nerve compression.

A

May be associated with hip fracture, dislocation or repair.
There is sensory loss over the posterior aspect of the thigh, gluteal regions and entire lower leg (medial calf and arch may be spared). The ankle jerk is lost while the knee jerk is preserved.

54
Q

Posterior tibial nerve compression

A

Aching or burning over the sole of the foot, positive Tinel’s sign over the nerve and sensory loss over the sole of foot.

55
Q

Lambert Eaton Myasthenic Syndrome

A

An autoimmune disease in which antibodies are directed against the presynaptic voltage-gated calcium channels.
It can occur sporadically or as part of a paraneoplastic syndrome.
Usually presents with proximal weakness, > in legs than arms. Like MG, weakness is exacerbated by exercise and heat.
Autonomic dysfunction in 75% of patients.
Ocular and bulbar muscles affected less than in MG and legs are less commonly affected in MG.

56
Q

Tay-Sachs disease

A

GM2 gangliosidosis or hexosaminidase A deficiency
Autosomal recessive
Progressive deterioration of mental and physical abilities.

57
Q

Pathophysiology in synucleinopathies

A

PD, Dementia with Lewy bodies, MSA
Aggregation, deposition and dysfunction of alpha-synuclein (aSyn) in Lewy bodies and glial cytoplasmic inclusions are common events.

58
Q

MSA

A

Heterogenous combination of autonomic failure, urogenital dysfunction, cerebellar ataxia, parkinsonian and pyramidal signs.
Diagnosis of probably MSA requires the presence of urinary dysfunction or orthostatic hypotension as well as a motor syndrome that includes parkinsonism with a poor response to levodopa or a cerebellar syndrome.

59
Q

Hypokalaemia and Hyperkalaemia Periodic Paralysis

A

Hyperkalaemic periodic paralysis: caused by a defect of sodium channel SCN4A, precipitated by rest following exercise, stress or ingesting certain foods.

Hypokalaemic periodic paralysis: caused by a defect in calcium channel CACNL1A3 and is precipitated by the partaking of meals high in carbohydrates, rest following exercise and excitement.

Exclude other causes.

60
Q

The first presentation of a patient with new Creutzfeldt-Jakob disease is likely to be with:

A

Psychiatric symptoms

Neurology (1 decks)

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