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
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
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
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
5
Q
Classification of aphasia?
A
6
Q
Cause of gait ataxia?
A
Cerebellar vermis lesions
7
Q
Cause of peripheral (‘finger-nose ataxia’)?
A
Cerebellar hemisphere lesions
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
9
Q
Clinical features of autonomic dysreflexia?
A
- extreme hypertension
- flushing
- sweating above the level of the cord lesion
- agitation
- untreated cases»_space; severe consequences of extreme hypertension have been reported, e.g. haemorrhagic stroke
10
Q
Erb-Duchenne paralysis?
A
> > Brachial plexus injury
- damage to C5,6 roots
- winged scapula
- may be caused by a breech presentation
11
Q
Klumpke’s paralysis?
A
> > Brachial plexus injury
- damage to T1
- loss of intrinsic hand muscles
- due to traction
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
13
Q
Tumours that most commonly spread to the brain?
A
- lung (most common)
- breast
- bowel
- skin (namely melanoma)
- kidney
14
Q
Most common primary brain tumour in adults?
A
Glioblastoma multiforme
15
Q
Imaging - solid tumour with central necrosis and a rim that enhances with contrast, with vasogenic oedema (disruption of BBB)?
A
Glioblastoma multiforme
16
Q
Histology - Pleomorphic tumour cells border necrotic areas?
A
Glioblastoma multiforme
17
Q
Histology - Spindle cells in concentric whorls and calcified psammoma bodies?
A
Meningioma
18
Q
Clinical features of vestibular schwannoma?
A
- hearing loss
- facial nerve palsy (due to compression of the nearby facial nerve)
- tinnitus
19
Q
Histology - Antoni A or B patterns. Verocay bodies (acellular areas surrounded by nuclear palisades)?
A
Vestibular schwannoma
20
Q
Most common primary brain tumour in children?
A
Pilocytic astrocytoma
21
Q
Histology - Rosenthal fibres (corkscrew eosinophilic bundle)?
A
Pilocytic astrocytoma
22
Q
Histology - Small, blue cells. Rosette pattern of cells with many mitotic figures?
A
Medulloblastoma
23
Q
Histology - perivascular pseudorosettes?
A
Ependymoma
24
Q
Histology - Calcifications with ‘fried-egg’ appearance?
A
Oligodendroma
25
Histology - foam cells and high vascularity?
Haemangioblastoma
26
Clinical features of craniopharyngioma?
- hormonal disturbance
- symptoms of hydrocephalus
- bitemporal hemianopia
27
Histology - Derived from remnants of Rathke pouch?
Craniopharyngioma
28
CT - well-circumscribed appearance with contrast enhancement?
Meningioma
29
Clinical features of Brown-Sequard syndrome?
>>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
Clinical features of cerebellar disease?
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
Most common hereditary peripheral neuropathy?
Charcot-Marie-Tooth disease
32
Clinical features of Charcot-Marie-Tooth disease?
- 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
Investigations for cluster headaches?
MRI with gadolinium contrast
34
Management of cluster headaches?
>>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
Characteristic feature of a common peroneal nerve lesion?
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
Clinical features of CJD?
dementia (rapid onset)
myoclonus
37
Investigations for CJD?
- CSF is usually normal
- EEG: biphasic, high amplitude sharp waves (only in sporadic CJD)
- MRI: hyperintense signals in the basal ganglia and thalamus
38
Classification of CJD?
*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
Clinical features of central venous thrombosis (CVT)?
- 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
Investigations for CVT?
MRI with venography is the preferred imaging modality
>>If this is not available cranial CT or CT venography can also be used.
41
Management of CVT?
**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
Clinical features of cervical spondylitic myelopathy?
- 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
Investigations for cervical spondylitic myelopathy?
MRI of the cervical spine is the gold standard test
44
Management of
>>Referred for assessment by specialist spinal services (neurosurgery or orthopaedic spinal surgery)
- decompressive surgery
- close observation is an option for mild stable disease
45
Clinical features of chronic inflammatory demyelinating polyneuropathy?
- distal and proximal weakness with sensory deficits developing over at least 8 weeks
46
Investigations of chronic inflammatory demyelinating polyneuropathy?
- 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
Management of chronic inflammatory demyelinating polyneuropathy?
>> 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
Starting antiepileptics after the first seizure?
- 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
Management generalised seizures?
Sodium valproate
50
Management focal seizures?
1st = lamotrigine
2nd = carbamazepine
51
carbamazepine may exacerbate?
absence seizures / myoclonic seizures
52
first-line management option for female patients experiencing tonic or atonic seizures?
lamotrigine
53
management of absence seizures?
ethosuximide
54
management of myoclonic seizures?
males: sodium valproate
females: levetiracetam
55
management of tonic / atonic seizures?
males: sodium valproate
females: lamotrigine
56
