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YEAR 6 > MED: Neurology > Flashcards

MED: Neurology Flashcards

1
Q

Wernicke’s aphasia?

A

> > Receptive

  • Due to a lesion of the superior temporal gyrus. It is typically supplied by the inferior division of the left MCA
  • Lesions result in sentences that make no sense, word substitution and neologisms but speech remains fluent - ‘word salad’
  • Comprehension is impaired
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2
Q

Broca’s aphasia?

A

> > Expressive

  • Due to a lesion of the inferior frontal gyrus. It is typically supplied by the superior division of the left MCA
  • Speech is non-fluent, laboured, and halting. Repetition is impaired
  • Comprehension is normal
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3
Q

Conduction aphasia?

A
  • Classically due to a stroke affecting the arcuate fasiculus - the connection between Wernicke’s and Broca’s area
  • Speech is fluent but repetition is poor. Aware of the errors they are making
  • Comprehension is normal
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4
Q

Global aphasia?

A
  • Large lesion affecting all 3 of the above areas resulting in severe expressive and receptive aphasia
  • May still be able to communicate using gestures
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5
Q

Classification of aphasia?

A
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6
Q

Cause of gait ataxia?

A

Cerebellar vermis lesions

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7
Q

Cause of peripheral (‘finger-nose ataxia’)?

A

Cerebellar hemisphere lesions

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8
Q

Features of ataxia telangiectasia?

A
  • cerebellar ataxia
  • telangiectasia (spider angiomas)
  • IgA deficiency resulting in recurrent chest infections
  • 10% risk of developing malignancy, lymphoma or leukaemia, but also non-lymphoid tumours
  • autosomal recessive
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9
Q

Clinical features of autonomic dysreflexia?

A
  • extreme hypertension
  • flushing
  • sweating above the level of the cord lesion
  • agitation
  • untreated cases&raquo_space; severe consequences of extreme hypertension have been reported, e.g. haemorrhagic stroke
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10
Q

Erb-Duchenne paralysis?

A

> > Brachial plexus injury

  • damage to C5,6 roots
  • winged scapula
  • may be caused by a breech presentation
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11
Q

Klumpke’s paralysis?

A

> > Brachial plexus injury

  • damage to T1
  • loss of intrinsic hand muscles
  • due to traction
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12
Q

Management of brain abscess?

A
  • surgery - craniotomy performed and abscess cavity debrided, may reform because the head is closed following abscess drainage
  • IV antibiotics: IV 3rd-generation cephalosporin + metronidazole
  • intracranial pressure management: e.g. dexamethasone
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13
Q

Tumours that most commonly spread to the brain?

A
  • lung (most common)
  • breast
  • bowel
  • skin (namely melanoma)
  • kidney
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14
Q

Most common primary brain tumour in adults?

A

Glioblastoma multiforme

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15
Q

Imaging - solid tumour with central necrosis and a rim that enhances with contrast, with vasogenic oedema (disruption of BBB)?

A

Glioblastoma multiforme

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16
Q

Histology - Pleomorphic tumour cells border necrotic areas?

A

Glioblastoma multiforme

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17
Q

Histology - Spindle cells in concentric whorls and calcified psammoma bodies?

A

Meningioma

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18
Q

Clinical features of vestibular schwannoma?

A
  • hearing loss
  • facial nerve palsy (due to compression of the nearby facial nerve)
  • tinnitus
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19
Q

Histology - Antoni A or B patterns. Verocay bodies (acellular areas surrounded by nuclear palisades)?

A

Vestibular schwannoma

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20
Q

Most common primary brain tumour in children?

A

Pilocytic astrocytoma

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21
Q

Histology - Rosenthal fibres (corkscrew eosinophilic bundle)?

A

Pilocytic astrocytoma

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22
Q

Histology - Small, blue cells. Rosette pattern of cells with many mitotic figures?

A

Medulloblastoma

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23
Q

Histology - perivascular pseudorosettes?

A

Ependymoma

24
Q

Histology - Calcifications with ‘fried-egg’ appearance?

A

Oligodendroma

25
Q

Histology - foam cells and high vascularity?

A

Haemangioblastoma

26
Q

Clinical features of craniopharyngioma?

A
  • hormonal disturbance
  • symptoms of hydrocephalus
  • bitemporal hemianopia
27
Q

Histology - Derived from remnants of Rathke pouch?

A

Craniopharyngioma

28
Q

CT - well-circumscribed appearance with contrast enhancement?

A

Meningioma

29
Q

Clinical features of Brown-Sequard syndrome?

A

> > Caused by lateral hemisection of the spinal cord

  • ipsilateral weakness below lesion
  • ipsilateral loss of proprioception and vibration sensation
  • contralateral loss of pain and temperature sensation
30
Q

Clinical features of cerebellar disease?

A

DANISH:

D - Dysdiadochokinesia, Dysmetria (past-pointing), patients may appear ‘Drunk’
A - Ataxia (limb, truncal)
N - Nystamus (horizontal = ipsilateral hemisphere)
I - Intention tremour
S - Slurred staccato speech, Scanning dysarthria
H - Hypotonia

31
Q

Most common hereditary peripheral neuropathy?

A

Charcot-Marie-Tooth disease

32
Q

Clinical features of Charcot-Marie-Tooth disease?

A
  • There may be a history of frequently sprained ankles
  • Foot drop
  • High-arched feet (pes cavus)
  • Hammer toes
  • Distal muscle weakness
  • Distal muscle atrophy
  • Hyporeflexia
  • Stork leg deformity
33
Q

Investigations for cluster headaches?

A

MRI with gadolinium contrast

34
Q

Management of cluster headaches?

A

> > Seek specialist advice from a neurologist

acute:

  • 100% oxygen
  • SC triptan

prophylaxis:

  • verapamil is the drug of choice
  • some evidence to support a tapering dose of prednisolone
35
Q

Characteristic feature of a common peroneal nerve lesion?

A

Foot drop

Also:

  • weakness of foot dorsiflexion
  • weakness of foot eversion
  • weakness of extensor hallucis longus
  • sensory loss over the dorsum of the foot and the lower lateral part of the leg
  • wasting of the anterior tibial and peroneal muscles
36
Q

Clinical features of CJD?

A

dementia (rapid onset)
myoclonus

37
Q

Investigations for CJD?

A
  • CSF is usually normal
  • EEG: biphasic, high amplitude sharp waves (only in sporadic CJD)
  • MRI: hyperintense signals in the basal ganglia and thalamus
38
Q

Classification of CJD?

A

Sporadic CJD

  • most common
  • mean age of onset is 65 years

New variant CJD:

  • younger patients (average age of onset = 25 years)
  • psychological symptoms such as anxiety, withdrawal and dysphonia are most common presenting features
39
Q

Clinical features of central venous thrombosis (CVT)?

A
  • Isolated intracranial hypertension - headache, often worse with positional or postural changes
  • Papilloedema and visual disturbances
  • Focal neurological abnormalities - may include motor weakness (e.g. hemiparesis), fluent aphasia; and sensory/visual field defects
  • Seizures - focal and generalised seizures may occur, as may status epilepticus.
  • Encephalopathy - typically seen in severe cases of CVT or with straight sinus thrombosis - causes reduced GCS, cognitive dysfunction and delirium/confusion
40
Q

Investigations for CVT?

A

MRI with venography is the preferred imaging modality

> > If this is not available cranial CT or CT venography can also be used.

41
Q

Management of CVT?

A

Acute antithrombotic therapy:

  • Low molecular weight heparin or unfractionated heparin
  • Small number of patients who have large and extensive CVT disease, or who do not improve with anticoagulation, go on to receive fibrinolysis
  • Patients who still deteriorate despite optimal anticoagulation may require surgical thrombectomy, although this is rare
  • Certain patients who have severe disease resulting in brain herniation or large haematomas may need decompressive surgery, but again this is rare

Acute symptom management:

  • Raised ICP - bed elevated, osmotic therapy (mannitol or hypertonic saline) administered and be hyperventilated in ICU
  • Brain herniation - may need emergency decompressive surgery
  • Seizures - anticonvulsants can be used both to treat seizures, and also as prophylaxis against seizures in patients deemed at high risk on neuroimaging review (large areas of cerebral oedema or infarction)
  • Infection/inflammation - antibiotic treatment for infection and glucocorticoid therapy for those with inflammatory disorders is often used

Long-term management:

  • Long-term anticoagulation with warfarin with an INR target of 2.5. This is for 3-6 months in provoked CVT and 6-12 months in those with an unprovoked CVT.
  • Women who previously were taking the COCP will need advice regarding non-oestrogen methods of contraception such as the POP. Women who developed an CVT whilst pregnant will need prophylactic anticoagulation during future pregnancies.
  • Patients may require rehabilitation due to residual deficits.
42
Q

Clinical features of cervical spondylitic myelopathy?

A
  • variety of motor weakness, sensory loss and bladder/bowel dysfunction
  • neck pain
  • wide-based, ataxic or spastic gait
  • upper motor neuron weakness in the lower legs - increased reflexes, increased tone and upgoing plantars
  • bladder dysfunction e.g. urgency, retention
43
Q

Investigations for cervical spondylitic myelopathy?

A

MRI of the cervical spine is the gold standard test

44
Q

Management of

A

> > Referred for assessment by specialist spinal services (neurosurgery or orthopaedic spinal surgery)

  • decompressive surgery
  • close observation is an option for mild stable disease
45
Q

Clinical features of chronic inflammatory demyelinating polyneuropathy?

A
  • distal and proximal weakness with sensory deficits developing over at least 8 weeks
46
Q

Investigations of chronic inflammatory demyelinating polyneuropathy?

A
  • Sensory and motor nerve conduction studies, performed bilaterally
  • Lumbar puncture - elevated CSF protein with leukocyte count <10/mm3 supports the diagnosis of CIDP
  • MR imaging - gadolinium enhancement and/or hypertrophy of the cauda equina, lumbosacral or cervical nerve roots, or the brachial or lumbosacral plexuses supports CIDP diagnosis.
  • Nerve biopsy - evidence of demyelination and/or remyelination by electron microscopy of nerve biopsy supports CIDP diagnosis
47
Q

Management of chronic inflammatory demyelinating polyneuropathy?

A

> > Mild symptoms / do not interfere with AODL may be observed without treatment initially

In those requiring treatment:

  • Corticosteroids - 60mg OD oral prednisolone for 6 weeks recommended as first line
  • Plasma exchange - effective for quick relief of symptoms, but requires combining with other treatments to demonstrate longer term benefits.
  • IVIG
  • Analgesia for neuropathic pain - e.g. gabapentin, pregabalin if this contributes a significant part of their symptoms.
48
Q

Starting antiepileptics after the first seizure?

A
  • the patient has a neurological deficit
  • brain imaging shows a structural abnormality
  • the EEG shows unequivocal epileptic activity
  • the patient or their family or carers consider the risk of having a further seizure unacceptable
49
Q

Management generalised seizures?

A

Sodium valproate

50
Q

Management focal seizures?

A

1st = lamotrigine
2nd = carbamazepine

51
Q

carbamazepine may exacerbate?

A

absence seizures / myoclonic seizures

52
Q

first-line management option for female patients experiencing tonic or atonic seizures?

A

lamotrigine

53
Q

management of absence seizures?

A

ethosuximide

54
Q

management of myoclonic seizures?

A

males: sodium valproate
females: levetiracetam

55
Q

management of tonic / atonic seizures?

A

males: sodium valproate
females: lamotrigine

56
Q
A

YEAR 6 (14 decks)

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