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NEUROLOGY Flashcards

1
Q

what are the complications of bacterial meningitis?

A
  • Sensorineural hearing loss (most common).
  • Cerebral infarction.
  • Seizures.
  • Cognitive impairment.
  • Motor deficits.
  • Hydrocephalus.
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2
Q

what are the clinical features of bacterial meningitis?

A
  • Headache.
  • Neck stiffness.
  • Fever.
  • Altered consciousness.
  • Vomiting.
  • Confusion.
  • Photophobia.
  • Seizures.
  • Petechial rash in meningococcal disease (red or purple non-blanching macules smaller than 2 mm)
  • Haemorrhagic rash in meningococcal disease (blanching macules larger than 2mm) which is absent in early phase and indicative of progression.
  • Kernig’s sign (unable to fully extend at knee when hip is flexed).
  • Brudzinski’s sign (person’s knees and hips flex when neck is flexed).
  • Children present with non-specific symptoms such as fever, vomiting, and irritability.
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3
Q

how should suspected meningococcal disease be managed pre-hospital?

A
  • Arrange emergency medical transfer to hospital by telephoning 999.
  • Give parenteral antibiotics (intravenous benzylpenicillin 1200 mg or cefotaxime 1g) when a non-blanching rash is present and meningococcal disease is suspected.
  • Do not give parenteral antibiotic treatment when a non-blanching rash is absent and suspected bacterial meningitis is suspected.
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4
Q

what investigations should be performed in suspected bacterial meningitis?

A
  • blood cultures
  • CT head
  • lumbar puncture
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5
Q

what are the CSF features of bacterial meningitis?

A
  • Opening CSF pressure: Raised.
  • Appearance: Turbid; Cloudy; Purulent.
  • WCC: Raised; Predominantly neutrophils.
  • CSF protein: Raised.
  • CSF glucose: Very low.
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6
Q

what are the contraindications to lumbar puncture in bacterial meningitis?

A
  • meningococcal meningitis diagnosed clinically
  • space occupying lesion on CT
  • signs of raised ICP
  • local infection
  • coagulation abnormalities
  • respiratory insufficiency
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7
Q

how is bacterial meningitis managed?

A
  • IV dexamethasone
  • IV ceftriaxone in adults and children older than 3 months
  • IV cefotaxime and amoxicillin in children under 3 months
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8
Q

what are the clinical features of viral meningitis?

A
  • Headache.
  • Nausea and vomiting.
  • Photophobia.
  • Neck stiffness.
  • Fever.
  • Rash (maculopapular rash with echovirus-9).
  • Kernig’s sing.
  • Brudzinski’s sing.
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9
Q

what are the CSF features of viral meningitis?

A
  • Opening pressure: Normal.
  • Appearance: Clear.
  • CSF WBC: Elevated; Predominantly lymphocytes.
  • CSF protein: Normal may be elevated.
  • CSF glucose: Normal may be low.
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10
Q

how is viral meningitis managed?

A
  • Offer empirical antibiotic therapy and dexamethasone for acute ill patients as the presentation may be indistinguishable from that of acute bacterial meningitis.
  • Offer supportive care (hydration, antipyretics, anti-emetics, analgesia) for confirmed enterovirus infection.
  • Offer aciclovir plus supportive care for confirmed HSV or varicella zoster infection.
  • Offer ganciclovir plus supportive care
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11
Q

what are the clinical features of fungal meningitis?

A
  • Progressive headache over several weeks.
  • Severe headache.
  • Nuchal rigidity (impaired neck flexion).
  • Photophobia.
  • Reduced visual acuity and papilloedema.
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12
Q

what are the CSF features of fungal meningitis?

A
  • CSF opening pressure = raised.
  • CSF appearance = Clear or cloudy.
  • CSF WCC = Raised; Predominantly lymphocytes.
  • CSF protein = Raised.
  • CSF glucose = Low.
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13
Q

how is fungal meningitis managed?

A
  • Offer induction combination therapy (amphotericin B and flucytosine) for 2 weeks.
  • Offer immediate initiation of antiretroviral therapy inpatients with HIV
  • Consider ventriculoperitoneal shunt if CSF opening pressure exceeds 20 cm H2O.
  • Offer consolidation therapy (fluconazole) for 8 weeks to prevent relapse.
  • Offer long-term maintenance therapy (fluconazole) for 1 year for HIV-associated cryptococcal meningitis following consolidation therapy.
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14
Q

what are the clinical features of tuberculous meningitis?

A
  • Vague headache.
  • Neck stiffness.
  • Vomiting.
  • Drowsiness.
  • Focal signs (diplopia, papilloedema, hemiparesis).
  • Seizures.
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15
Q

what are the CSF features of tuberculous meningitis?

A
  • CSF opening pressure = Raised.
  • Appearance: Clear or cloudy.
  • CSF ECC: Raised; Predominantly lymphocytes.
  • CSF protein: Markedly raised.
  • CSF glucose : Very low.
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16
Q

how is tuberculous meningitis managed?

A
  • Offer treatment with antituberculosis drugs (rifampicin, isoniazid and pyrazinamide) for 10 months. Ethambutol should be avoided because of the eye complications.
  • Offer adjunct corticosteroids (prednisolone 60 mg) for 3 weeks.
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17
Q

what is encephalitis?

A

inflammation of the brain parenchyma

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18
Q

what are the risk factors for encephalitis?

A
  • Age <1 or >65
  • Immunodeficiency
  • Post-infection
  • Exposure to blood or bodily fluid
  • Organ transplant
  • Animal or insect bites
  • Location
  • Season
  • Swimming or diving in warm freshwater or nasal/sinus irrigation
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19
Q

what are the clinical features of encephalitis?

A
  • Fever
  • Rash
  • Altered mental state
  • Focal neurological deficit
  • Meningismus
  • Parotitis in mumps
  • Lymphadenopathy
  • Optic neuritis
  • Acute flaccid paralysis
  • Movement disorder
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20
Q

how is encephalitis managed?

A
  • Give acyclovir and supportive care if viral aetiology is suspected in an immunocompetent patient
  • If the patient is immunocompromised, give ganciclovir, foscarnet and acyclovir
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21
Q

how is non-viral encephalitis managed?

A
  • Add immune-modulating therapy with methylprednisolone, IV immunoglobulin or plasma exchange in autoimmune, ADEM and paraneoplastic encephalitis
  • Add benzylpenicillin if confirmed syphilis encephalitis
  • Add ampicillin and gentamicin if listeria
  • Add doxycycline or erythromycin with immune modulation if mycoplasma
  • Add doxycycline if confirmed rocky mountain spotted fever encephalitis
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22
Q

what are the risk factors for neurocysticercosis?

A
  • Living on a farm
  • Poor hygiene
  • Eating or handling undercooked meat, fish or crustaceans
  • Ingestion of contaminated water
  • Dog owners
  • Children
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23
Q

what are the clinical features of neurocysticercosis?

A
  • Visible worm segments in stool
  • Features of raised intracranial pressure and seizures
  • Hepatomegaly
  • Cough with haemoptysis
  • Anaemia
  • Allergy symptoms due to lesional rupture
  • Headaches and visual disturbances
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24
Q

how is neurocysticercosis diagnosed?

A
  • Perform a stool examination: eggs and proglottids in stool
  • Perform an enzyme-linked immunoelectrotransfer blot: Taenia solium with purified glycoprotein antigens
  • Perform CT head: Brain calcification
  • Perform MRI brain: extraparenchymal cysticerci tapeworm scolex and ring enhancing lesions
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25
Q

how is neurocysticercosis managed?

A
  • IV dexamethasone
  • albendazole
  • anti-convulsants
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26
Q

what are the clinical features of cluster headaches?

A
  • Pain location: Unilateral peri-orbital pain associated.
  • Pain quality: Most often reported as sharp but this is variable.
  • Pain intensity: Severe or very severe.
  • Effects on activities: Restlessness or agitation.
  • Conjunctival injection
  • Lacrimation
  • Eyelid oedema
  • Forehead and facial sweating
  • Constricted pupil and eyelid drooping
  • Nasal congestion.
  • Duration: 15 minutes to 180 minutes.
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27
Q

how is an acute episode of cluster headache managed?

A
  • Offer 100% oxygen at a flow rate of least 12 litres per minute with a non-rebreathing mask and reservoir mask. Arrange provision of home and ambulatory oxygen.
  • Offer subcutaneous triptan (sumatriptan).
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28
Q

what prophylactic treatments can be offered to patients with cluster headaches?

A
  • Consider verapamil for prophylactic treatment during a bout of cluster headache.
  • Consider topiramate or lithium as a second line prophylactic treatment during a bout of cluster headaches.
  • Consider gammaCore to reduce the frequency and intensity of cluster headaches.
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29
Q

what are the features of medication overuse headaches?

A
  • Headache occurs on 15 or more days per month
  • regular overuse of symptomatic headache medication for more than 3 months
  • For triptans, opioids, ergotamine and combination analgesia, intake must be 10 days or more per months to be considered overuse.
  • For simple analgesics such as NSAIDs, aspirin, and paracetamol, intake must be 15 days or more per month to be considered overuse.
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30
Q

how is medication overuse headache managed?

A
  • Advise people to stop taking all overused acute headache medications for at least 1 month and to stop abruptly rather than gradually.
  • Review and reassess the underlying primary headache disorder 4–8 weeks after withdrawing the overused medication.
  • If appropriate, the overused medications may be reintroduced after 2 months, with clear restrictions on frequency of use.
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31
Q

what are the risk factors for migraine?

A
  • Family history of migraine.
  • Disturbed sleep.
  • Irregular or missed meals.
  • Excessive caffeine intake.
  • Lack of exercise.
  • Menstruation.
  • Obesity.
  • Stressful life events.
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32
Q

what are the clinical features of migraine without aura?

A
  • Headache lasting 4-72 hours in adults or 2-72 hours in adolescents.
  • Unilateral location, more common bilateral in children.
  • Pulsating quality described as throbbing or banging.
  • Moderate or severe pain intensity.
  • Aggravation by, or causing avoidance of routine activities.
  • Headache with associated symptoms include at least one of:
  • –Nausea and vomiting.
  • –Photophobia and photophobia.
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33
Q

what are the clinical features of migraine with aura?

A
  • Visual symptoms such as zigzag lines (positive symptom) and scotoma (negative symptom).
  • Sensory symptoms such as unilateral pins and needles or numbness.
  • Speech and language symptoms such as dysphagia.
  • At least three of the following:
  • –At least one aura symptoms spreads gradually over at least 5 minutes.
  • –Two or more aura symptoms occur in succession.
  • –Each individual aura symptom lasts 5-60 minutes and is fully reversible.
  • –At least one aura symptom is unilateral.
  • –At least one aura symptom is positive.
  • –The aura is accompanied, or followed within 60 minutes, by headache.
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34
Q

what is the reliever management of migraine?

A
  • Encourage the patient to keep a headache diary to identify triggers to be avoided and to review the effectiveness of treatment.
  • Recommend lifestyle changes
  • Offer simple analgesia
  • Trpitan
  • antiemetic
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35
Q

what is the prophylactic management of migraine?

A
  • topiramate (not in pregnancy)
  • propranolol
  • amitriptyline
  • propranolol or pizotifen in children
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36
Q

what are the clinical features of neuroblastoma?

A
  • Abdominal distention
  • Abdominal mass
  • Pain: abdominal with a mass, but there may be bone or back pain indicative of metastases
  • Decreased appetite
  • Weight loss
  • Fatigue
  • Periorbital ecchymosis and subcutaneous skin nodules associated with metastases
  • Signs of Horner’s syndrome if primary is in the upper portion of the thoracic outlet of cervical sympathetic chain
  • Signs of superior vena cava syndrome if the primary is in the upper portion of the thoracic outlet
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37
Q

how is neuroblastoma diagnosed?

A
  • Measure urinary catecholamines: Positive
  • Perform ultrasound abdomen: heterogenous mass with internal vascularity; may show calcifications or areas of necrosis
  • Perform CT or MRI abdomen: heterogenous mass; may show calcifications or areas of necrosis
  • Consider performing 123-iodine-metaiodobenzylguanidine (MIBG) scintigraphy or PET with 18-F-deoxyglucose to identify sites of metastases
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38
Q

define stage 1 neuroblastoma

A

localised tumour with complete gross excision, with or without microscopic residual disease

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39
Q

define stage 2a neuroblastoma

A

localised tumour with incomplete gross excision

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40
Q

define stage 2b neuroblastoma

A
  • localised tumour with or without complete gross excision

- with ipsilateral non-adherent lymph nodes positive for tumour

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41
Q

define stage 3 neuroblastoma

A
  • unresectable unilateral tumour infiltrating across the midline
  • with or without regional lymph node involvement
  • localised unilateral tumour with contralateral regional lymph node involvement
  • midline tumour with bilateral extension via infiltration or lymph node involvement
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42
Q

define stage 4 neuroblastoma

A

any primary tumour with dissemination to distant lymph nodes, bone, bone marrow, liver, skin, and/or other organs

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43
Q

define stage 4s neuroblastoma

A

localised primary tumour, with dissemination limited to skin, liver, and/or bone marrow (limited to infants <1 year of age, marrow involvement <10% of total nucleated cells, 123-iodine-metaiodobenzylguanidine [MIBG] scan findings negative in the marrow).

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44
Q

how is low risk neuroblastoma managed?

A

-perform surgical tumour resection

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45
Q

how is intermediate risk neuroblastoma managed?

A

0neo-adjuvant chemotherapy with carboplatin, etoposide, cyclophosphamide and doxorubicin

  • surgery
  • radiotherapy if resection is unsuccessful
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46
Q

how is high risk neuroblastoma managed?

A
  • give induction chemotherapy with carboplatin, etoposide, cyclophosphamide and doxorubicin
  • surgical resection
  • consolidation chemotherapy with carboplatin, etoposide, cyclophosphamide, melphalan, busulfan or thiotepa followed by autologous bone marrow transplant
  • Local control of the tumour is achieved with radiotherapy
  • dinutuximab beta.
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47
Q

what are the clinical features of a frontal lobe glioma?

A
  • personality change
  • cognitive changes
  • emotional lability
  • productive dysphasia
  • motor weakness
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48
Q

what are the clinical features of a temporal lobe glioma?

A
  • contralateral homonymous upper quandrantinopia

- receptive aphasia

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49
Q

what are the clinical features of a parietal lobe glioma?

A
  • sensory deficit

- contralateral homonymous lower quadrantinopia

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50
Q

what are the clinical features of an occipital lobe glioma?

A

-contralateral homonymous hemianopia

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51
Q

what are the clinical features of a cerebellar glioma?

A

-truncal ataxia

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52
Q

how are gliomas graded using MRI?

A
  • Grade 1: Well circumscribed.
  • Grade 2: Well defined margins; Hyper-intense T1; Hypo-intense T2.
  • Grade 3: Poorly defined markings; Hypo-intense T1; Hyper-intense T2.
  • Grade 4 (glioblastoma) Poorly defined; Significant oedema; necrosis.
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53
Q

how are gliomas managed?

A
  • dexamethasone and mannitol for raised ICP
  • levetiracetam for seizures
  • maximal resection
  • maximal safe resection plus radiotherapy (60 Gy) for accessibly grade 2 and 3 tumours. For inaccessible tumours offer radiotherapy.
  • maximal safe resection plus radiotherapy plus chemotherapy (temozolomide) for accessible grade 4 tumours. For inaccessible tumours offer radiotherapy and chemotherapy.
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54
Q

what are the clinical features of meningiomas?

A
  • Headache.
  • Focal neurological deficits based on location and size of tumour.
  • Seizures
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55
Q

how are meningiomas managed?

A
  • surgical excision and adjunct stereotactic radiosurgery for symptomatic tumours in under 65s
  • stereotactic radiosurgery for symptomatic tumours in over 65s and poor surgical candidates.
  • salvage therapy for recurrent tumour following surgical resection or stereotactic radiosurgery.
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56
Q

what are the clinical features of acoustic neuromas?

A
  • Asymmetrical hearing loss, usually gradual
  • Facial numbness
  • Progressive episodes of dizziness
  • Tinnitus
  • Difficulty localising sounds
  • Symptoms associated with other cranial nerve palsies as the tumour enlarges
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57
Q

how are acoustic neuromas diagnosed?

A
  • audiogram: sensorineural hearing loss
  • gadolinium enhanced MRI head: uniformly enhanced, dense mass extending into the internal acoustic meatus; Absence of dural tail
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58
Q

how are acoustic neuromas managed?

A
  • observe
  • surgical resection
  • stereotactic radiotherapy
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59
Q

what are the risk factors for idiopathic intracranial hypertension?

A
  • Female sex.
  • Weight gain.
  • Obesity.
  • Drugs including the oral contraceptive pill, vitamin A, steroids, and indomethacin.
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60
Q

what are the clinical features of idiopathic intracranial hypertension?

A
  • Headache.
  • Visual field loss.
  • Pulse-synchronous headache.
  • Photophobia.
  • Decreased visual acuity.
  • Diplopia.
  • Sixth nerve palsy.
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61
Q

how is idiopathic intracranial hypertension diagnosed?

A
  • Perform perimetry: Enlarged blind spot.
  • Perform optic disc photographs: Papilloedema.
  • Perform a lumbar puncture: Elevated opening pressure.
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62
Q

how is idiopathic intracranial hypertension diagnosed?

A
  • Recommend weight reduction
  • carbonic anhydrase inhibitor (acetazolamide) to decrease intracranial pressure.
  • topiramate as a secondary option to decrease intracranial pressure.
  • CSF shunting for intractable headaches.
  • optic nerve sheath fenestration for patients with visual loss.
  • low dose amitriptyline for pain management.
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63
Q

what are the clinical features of subarachnoid haemorrhage?

A
  • Thunderclap headache, a sudden severe headache that peaks within 1 to 5 minutes and lasts more than an hour.
  • Vomiting.
  • Photophobia.
  • Neck stiffness.
  • Depressed consciousness.
  • Confusion.
  • Kernig’s sign.
  • Features of third nerve compression e.g. eyelid drooping, diplopia and mydriasis, orbital pain.
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64
Q

how is SAH diagnosed?

A

-Order an emergency non-contrast CT:
Hyper-dense areas of blood in the subarachnoid space and basal cisterns.

-CT/MR angiography to identify the causal pathology

-Perform a lumbar puncture: Bloody and xanthochromic
appearance

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65
Q

how is SAH managed?

A
  • ABC approach
  • nimodipine
  • analgesia and supportive care
  • reverse anticoagulation
  • endovascular coiling or surgical clipping
  • bed rest
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66
Q

what are the clinical features of subdural haematoma?

A
  • Headache.
  • Nausea and vomiting.
  • Drowsiness.
  • Confusion.
  • Otorrhoea and rhinorrhoea indicate occult basilar skull fracture.
  • Hemiparesis.
  • Localised weakness.
  • Loss of bowel and bladder continence.
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67
Q

how is subdural haematoma diagnosed?

A

-Perform non-contrast CT scan: Crescentic subdural fluid collection that can cross suture lines; Hyper-dense in acute SDH; Hypo-dense in chronic SDH.

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68
Q

how is acute subdural haematoma managed?

A
  • Perform a trauma craniotomy for acute subdural haematomas that are larger than 10 mm in size or midline shift greatest than 5 mm.
  • Offer prophylactic antiepileptics (phenytoin or levetiracetam)
  • Stop anti platelet or anticoagulant therapy.
  • Offer an intracranial pressure lowering regimen
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69
Q

how are chronic subdural haematomas managed?

A
  • Offer antiepileptics (phenytoin or levetiracetam)
  • Perform burr-hole craniotomy with irrigation or a test drill craniotomy with drain placement for symptomatic chronic haematoma.
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70
Q

what are the clinical features of extradural haemorrhage?

A
  • Head injury with a brief duration of unconsciousness, followed by improvement (the lucid interval).
  • Stupor
  • Ipsilateral dilated pupil
  • Contralateral hemiparesis, with rapid transtentorial coning.
  • Bilateral fixed dilated pupils, tetraplegia and respiratory arrest follow.
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71
Q

how is extradural haemorrhage managed?

A

-Perform a CT head: bi-convex hyperlucency limited by sutures; Features of mass effect such a midline shift, subfalcine and uncal herniation; swirl sign with ongoing bleeding

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72
Q

what are the clinical features of a cerebellar haemorrhage?

A
  • headache, often followed by stupor/coma and signs of cerebellar/brainstem origin (e.g. nystagmus, ocular palsies).
  • Gaze deviates towards the haemorrhage.
  • Skew deviation
  • acute hydrocephalus
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73
Q

what are the clinical features of tension type headache?

A
  • Location: Bilateral pain.
  • Pressing or tightening, non-pulsating.
  • Pain intensity: Mild to moderate.
  • Not aggravated by routine activities of daily living.
  • No nausea or vomiting
  • no more than one of photophobia or photophobia.
  • 30 minutes to continuous.
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74
Q

how is tension type headache managed?

A
  • simple analgesia (aspirin, paracetamol, ibuprofen) for an acute episode.
  • acupuncture (10 sessions over 5-8 weeks) for the prophylactic treatment of chronic tension-type headaches.
  • pharmacological prophylaxis (amitriptyline) taking into account comorbidities and risk of adverse effects, this is an ‘off-label’ indication.
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75
Q

what are the risk factors for BPPV?

A
  • Increasing age
  • Female sex
  • Head trauma
  • Prolonged recumbent position
  • Migraines
  • Inner ear surgery
  • Labrynthitis
  • Meniere’s disease
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76
Q

what are the clinical features of BPPV?

A
  • Vertigo provoked by specific head movements (looking up, bending down, getting up, turning the head and rolling over on one side).
  • Vertigo of <30 seconds
  • Nausea, imbalance and lightheaded feeling
  • No associated neurological or otological symptoms
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77
Q

how is BPPV diagnosed?

A

-dix hallpike

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78
Q

how is BPPV treated?

A
  • epley or semont

- brandt-daroff exercises

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79
Q

what are the clinical features of meniere’s disease?

A
  • Vertigo lasting minutes to hours
  • Hearing loss
  • Tinnitus, usually described as roaring
  • Aural fullness
  • Drop attacks
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80
Q

how is meniere’s disease managed?

A
  • short course of prochlorperazine, or an antihistamine (for example cinnarizine, cyclizine, or promethazine teoclate).
  • trial betahistine to reduce the frequency and severity of attacks of hearing loss, tinnitus, and vertigo.
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81
Q

what are the clinical features of vestibular neuritis?

A
  • Spontaneous, rotational vertigo that can develop on walking and worsens over the day
  • Exacerbated by changing head position, but initially is constant
  • Nausea and vomiting
  • Malaise, pallor and sweating
  • Falls due to affect on balance
  • Follows viral illness
  • Fine, horizontal nystagmus
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82
Q

how is vestibular neuritis managed?

A
  • To rapidly relieve severe nausea or vomiting associated with vertigo, consider giving buccal prochlorperazine, or an intramuscular injection of prochlorperazine or cyclizine.
  • To alleviate less severe nausea, vomiting, and vertigo, consider prescribing a short oral course of prochlorperazine, or an antihistamine (cinnarizine, cyclizine, or promethazine teoclate).
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83
Q

when should a patient with vestibular neuritis be referred to a balance specialist?

A
  • Symptoms are atypical
  • Symptoms persist with no improvement for more than one week during treatment
  • Symptoms last longer than 6 weeks
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84
Q

what are the risk factors for developing labyrinthitis?

A
  • Viral infections
  • Chronic suppurative otitis media
  • Acute otitis media
  • Cholesteatoma
  • Meningitis
  • Inner ear malformations
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85
Q

what are the clinical features of labyrinthitis?

A
  • Acute rotational vertigo lasting 72 hours
  • Nausea and vomiting
  • Hearing loss
  • Otorrhoea
  • Nystagmus
  • Tinnitus
  • Vertigo-related quick head or body movements
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86
Q

how is labyrinthitis managed?

A
  • To rapidly relieve severe nausea or vomiting associated with vertigo, consider giving buccal prochlorperazine, or an intramuscular injection of prochlorperazine or cyclizine.
  • To alleviate less severe nausea, vomiting, and vertigo, consider prescribing a short oral course of prochlorperazine, or an antihistamine (cinnarizine, cyclizine, or promethazine teoclate).
  • If viral associated labyrinthitis with no HIV, give prednisolone for 10 to 14 days
  • In any other cause, give vestibular suppressants and anti-emetics and treat the underlying condition
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87
Q

what are the clinical features of Alzheimer’s?

A
  • Progressive memory loss: loss of recent memory first
  • Disorientation
  • Nominal dysphasia: Difficulties naming people and objects
  • Misplacing items and getting lost
  • Apathy: become more passive, sleep more than usual or not want to perform usual activities
  • Decline in activities of daily living and instrumental activities of daily living
  • Personality change
  • Poor abstract thinking
  • Construction dyspraxia
  • Prosopagnosia: failure to recognise faces
  • Autoprosopagnosia: failure to recognise oneself in the mirror
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88
Q

how is Alzheimer’s dementia diagnosed?

A
  • bedside cognitive testing
  • rule out reversible causes
  • perform MRI head, FDG-PET or perfusion SPECT
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89
Q

how is Alzheimer’s managed?

A
  • acetylcholinesterase inhibitors

- memantine

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90
Q

what are the risk factors for vascular dementia?

A
  • Male
  • Age >60 years
  • Obesity
  • Hypertension
  • Cigarette smoking
  • Diabetes mellitus
  • Hypercholesterolaemia
  • Alcohol abuse
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91
Q

what are the clinical features of vascular dementia?

A
  • History of stroke/TIA
  • Difficulty solving problems
  • Apathy
  • Disinhibition
  • Slowed processing of information
  • Poor attention
  • Retrieval memory deficit
  • Frontal release reflexes: including grasp, glabella tap and jaw-jerk.
  • Focal neurology and impaired gait and balance
  • Stepwise course of cognitive decline
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92
Q

how is vascular dementia diagnosed?

A
  • bedside cognitive testing
  • rule out reversible causes
  • CT/MRI head: vascular lesions
  • carotid duplex: carotid artery stenosis
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93
Q

how is vascular dementia managed?

A
  • manage vascular risk factors
  • Offer group cognitive stimulation therapy, group reminiscence therapy or occupational therapy to patients living with mild to moderate dementia
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94
Q

what are the clinical features of dementia with lewy bodies?

A
  • Cognitive fluctuations
  • Visual hallucinations: often take the form of people or animals or the sense of a presence (extracampine)
  • At least one Parkinsonism symptom
  • REM sleep behavioural disturbance
  • Autonomic dysfunction
  • Attention and visuospatial abnormalities
  • Delusions
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95
Q

how is dementia with lewy bodies diagnosed?

A
  • bedside cognitive testing
  • rule out reversible causes
  • MRI head: cortical atrophy with preservation of medial temporal lobe
  • SPECT/PET: low basal ganglia dopamine transporter uptake
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96
Q

how is dementia with lewy bodies managed?

A
  • donepezil or rivastigmine

- galatamine if not tolerated

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97
Q

what are the clinical features of frontotemporal dementia?

A
  • coarsening of personality: disregard for social conventions, slovenly appearance, impatience and irritability, argumentativeness, lewd and tactless remarks, child-like and impulsive actions, loss of empathy and concern for others, compulsions, and rigid adherence to routines.
  • Progressive loss of language fluency or comprehension
  • Development of memory impairment, disorientation or apraxia
  • Progressive self-neglect and abandonment of work, activities and social contacts
  • Inattentiveness, puerile pre-occupations, economy of effect and impulsive responding.
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98
Q

how is fronto-temporal dementia diagnosed?

A
  • bedside cognitive testing
  • rule out reversible causes
  • perform FDG-PET or perfusion SPECT: Focal hypo metabolism in the frontal and anterior temporal lobes
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99
Q

how is fronto-temporal dementia diagnosed?

A

-anti-psychotic as needed

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100
Q

what are the clinical features of prion diseases?

A
  • Cognitive impairment
  • Limb or gait ataxia
  • Myoclonus
  • Parkinsonism
  • Psychiatric symptoms
  • Visual changes
  • Insomnia and dysautonomia
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101
Q

how is prion disease dementia diagnosed?

A
  • brain MRI: demonstrates hyperintensity in the cerebral cortex, basal ganglia, and thalamus on diffusion-weighted imaging and FLAIR sequences; hypointensity (restricted diffusion) on attenuated diffusion coefficient map (ADC) sequences
  • EEG: generalised slowing, focal or diffuse and periodic poly spike wave complexes
  • quaking-induced conversion: positive
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102
Q

how are prion dementias managed?

A
  • Provide supportive care
  • Consider a benzodiazepine or antidepressant for mild to moderate anxiety and agitation
  • Consider a second generation anti-psychotic for moderate to severe agitation or psychosis
  • Consider a benzodiazepine or anti-convulsant for distressing myoclonus
  • Consider an SSRI for depression
  • Consider a hypnotic for insomnia
  • Give analgesia for skeletal muscle pain
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103
Q

what are the clinical features of Parkinson’s disease?

A
  • Bradykinesia
  • Resting, pill rolling tremor of 4-6Hz with asymmetrical onset
  • Cogwheel, lead pipe rigidity
  • Postural instability
  • Mask-like facies
  • Hypophonia
  • Micrographia
  • Stooped posture with shuffling gait
  • Conjugate gaze disorders
  • Features of autonomic neuropathy
  • Prodromal symptoms that occur approximately 7 years before diagnosis: anosmia, depression, anxiety, aches and pains, REM sleep disorder, autonomic features, constipation and restless leg syndrome
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104
Q

how is Parkinson’s disease diagnosed?

A
  • Parkinson’s disease is a clinical diagnosis: improvement in symptoms with a dopaminergic agent supports the diagnosis
  • Consider 123I FP CIT single photon emission computed tomography (SPECT) for people with tremor if essential tremor cannot be clinically differentiated from parkinsonism.
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105
Q

how is Parkinson’s disease managed?

A
  • levodopa/co-careldopa
  • dopamine agonists or MAO-B inhibitors if motor symptoms do not affect QoL
  • ergot derived drugs if dyskinesia or motor fluctuations not controlled by other drugs
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106
Q

how is advanced Parkinson’s managed?

A
  • intermittent apomorphine injection
  • continuous subcutaneous apomorphine infusion.
  • deep brain stimulation
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107
Q

how is Parkinson’s disease dementia managed?

A
  • rivastigmine

- memantine

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108
Q

define cardiac syncope

A

-syncope caused by bradycardia, tachycardia, or hypotension due to low cardiac index, blood flow obstruction, vasodilatation, or acute vascular dissection.

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109
Q

define non-cardiac syncope

A

is syncope due to a reflex that causes vasodilation, bradycardia, or both

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110
Q

what are the clinical features of vasovagal syncope?

A
  • A known precipitant e.g. fear, venesection, pain or prolonged standing
  • Dizziness and lightheadedness
  • Nausea
  • Sweating
  • Feeling hot
  • Visual grey out
  • Associated with standing too rapidly in orthostatic hypotension
  • Rapid recovery
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111
Q

what are the clinical features of cardiac syncope?

A
  • Little or no warning
  • May be associated with palpitations or chest pain
  • Can occur at rest or during exercise
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112
Q

what investigations should be perform in a patient with transient loss of consciousness?

A
  • 12 lead ECG
  • blood glucose
  • FBC
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113
Q

what is a tonic seizure?

A

-stiffening of muscles resulting in a fall

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114
Q

what is an atonic seizure?

A

-muscles suddenly relax, and they become floppy.

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115
Q

how are tonic/atonic seizures diagnosed?

A
  • EEG: atonic show rhythmic spike and wave complexes; tonic seizures show diffuse or generalised accelerating low amplitude activity
  • MRI
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116
Q

what is the first line treatment of tonic or atonic seizures?

A
  • sodium valproate

- lamotrigine

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117
Q

what are the signs of a LMN lesion?

A
  • Weakness
  • Wasting
  • Hypotonia
  • Reflex loss
  • Fasciculation
  • Fibrillation potentials on EMG
  • Muscle contractures
  • Trophic changes in skin and nails
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118
Q

what are the signs of an UMN lesion?

A
  • Upper limb extensor muscles weaker than flexors
  • Lower limb flexors weaker than extensor
  • Finer more skilful movements most severely impaired
  • spasticity
  • muscle wasting
  • hyperreflexia
  • positive babinski sign
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119
Q

what are the clinical features of MND?

A
  • Upper extremity weakness with difficulties of ADL
  • Stiffness with poor co-ordination and balance
  • Spastic, unsteady gait
  • Painful muscle spasms
  • Difficulties in rising from seated and climbing stairs
  • Foot drop
  • Head drop
  • Progressive difficulties in maintaining erect posture with stooping
  • Muscle atrophy
  • Increased lumbar lordosis and abdominal protuberance
  • Hyper-reflexia
  • Dyspnoea
  • Choking and coughing
  • Strained, slow speech
  • Slurred, nasal and dysphonic speech
  • Emotional incontinence associated with pseudobulbar palsy
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120
Q

how is MND diagnosed?

A
  • clinical diagnosis

- EMG: diffuse, ongoing, chronic denervation

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121
Q

how is MND managed?

A
  • riluzole
  • quinine, baclofen, tizanidine, dantrolene or gabapentin for muscle cramps
  • anti-muscarinic or glycopyrrolate for sialorrhoea
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122
Q

what are the clinical features of absence seizures?

A
  • Staring episode lasing 5 to 10 seconds with no aura and no post-ictal state
  • Childhood onset
  • Hyperventilation induced seizure
  • Simple automatisms
  • Recent decline in school performance
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123
Q

what is seen on EEG in absence seizures?

A

generalised 3Hz spike and wave

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124
Q

what is the first line management of absence seizures?

A
  • ethosuximide

- sodium valproate

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125
Q

what is the second line management of absence seizures?

A

-combine ethosuximide and lamotrigine or ethoxusimide and sodium valproate

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126
Q

what are the clinical features of generalised tonic-clonic seizures?

A
  • Focal neurological deficits may be present if there is an underlying cause for the epilepsy e.g. space occupying lesion
  • Loss of consciousness or awareness
  • Initial tonic stiffening followed by clonic phase with synchronous jerking of the limbs
  • Eyes remain open throughout
  • A post-ictal period of flaccid unresponsiveness
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127
Q

what is seen on EEG in generalised tonic clonic seizures?

A

generalised epileptiform activity

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128
Q

how are generalised tonic-clonic seizures managed?

A
  • sodium valproate
  • lamotrigine
  • consider carbamazepine or oxcarbazepine
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129
Q

what are the clinical features of focal epilepsy?

A
  • Movement of one side of the body or one specific body part
  • Premonitory sensation or experience (epigastric sensation, deja/jamais vu) in temporal lobe epilepsy
  • Temporary post-ictal hemiparesis (Todd’s Paresis)
  • Temporary aphasia and automatisms such as lip-smacking, picking at clothes or posturing
  • Staring and being unaware of surroundings
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130
Q

what is seen on EEG in focal seizures?

A

-focal spikes or sharp waves with associated slowing of the electrical activity in area of the spikes

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131
Q

how are focal seizures managed?

A
  • carbamazepine or lamotrigine

- second line: levetiracetam or oxcarbazepine or sodium valproate

132
Q

what are the clinical features of juvenile myoclonic epilepsy?

A

-jerking in the morning

133
Q

what are the EEG features of juvenile myoclonic epilepsy?

A

Generalised 4-6Hz polyspike and wave

134
Q

how are myoclonic seizures managed?

A
  • sodium valproate

- lamotrigine, levetiracetam, topiramate

135
Q

what are the clinical features of west syndrome?

A
  • Symmetrical, bilateral, brief spasms of the axial muscle groups occurring in clusters
  • Head nodding
  • Neurodevelopmental delay or regression
  • Abnormal eye movements
136
Q

what is seen on EEG in west syndrome?

A

hypsarrhythmia or modified hypsarrhythmia

137
Q

how is west syndrome managed?

A
  • prednisolone

- vigabatrin

138
Q

according to the Bamford criteria, what is a total anterior circulation stroke?

A

-All three of unilateral weakness and/or sensory deficit of the face, arm and leg, homonymous hemianopia and higher cerebral dysfunction (dysphasia, visuospatial disorder)

139
Q

according to the Bamford criteria, what is a partial anterior circulation stroke?

A

-Two of unilateral weakness and/or sensory deficit of the face, arm and leg, homonymous hemianopia and higher cerebral dysfunction

140
Q

according to the Bamford criteria, what is a posterior circulation stroke?

A

-one of cranial nerve palsy and a contralateral motor/sensory deficit, conjugate eye movement disorder, cerebellar dysfunction or isolated homonymous hemianopia or cortical blindness

141
Q

according to the Bamford criteria, what is a lacunar stroke?

A
  • one of pure sensory stroke, pure motor stroke, sensorimotor stroke or ataxic hemiparesis
142
Q

what are the clinical features of a TIA?

A
  • Sudden onset and brief duration of symptoms
  • Unilateral weakness or paralysis, which can occur in both anterior and posterior circulation TIAs
  • Bilateral limb weakness is a feature of vertebrobasilar ischaemia
  • Dysphasia in anterior circulation ischaemia
  • Ataxia, vertigo or loss of balance which is common in posterior circulation
  • Sudden transient loss of vision in one eye (Amaurosis Fugax)
  • Homonymous hemianopia in posterior circulation TIA
  • Diplopia in posterior circulation TIA
143
Q

how is a TIA managed?

A
  • Offer 300mg of oral aspirin
  • refer for specialist investigation within 24 hours
  • offer secondary prevention
144
Q

which patients with TIA should be considered for carotid endarterectomy?

A
  • carotid stenosis of 50 to 99% according to the NASCET criteria
  • 70% using ECST criteria
145
Q

what are the clinical features of status epilepticus?

A
  • Prolonged or repeated tonic-clonic seizures with an altered level of consciousness
  • Altered level of consciousness, confusion or change in personality with limited or absent motor findings
  • Presence of risk factors:
  • –Poor anti-convulsant adherence
  • –Alcohol use or withdrawal
  • –Disturbances in water, glucose or electrolyte metabolism
  • –Cortical structural damage
  • –Recreational drug use
146
Q

what investigations should be performed in status epilepticus?

A
  • blood glucose
  • ABG
  • U and E
  • anti-convulsant drug levels and toxicology
  • chest x-ray (aspiration post-ictus)
  • CT head
147
Q

how is convulsive status epilepticus managed in the community?

A
  • buccal midazolam or rectal diazepam/ IV lorazepam if IV access
  • secure airway
  • transfer to hospital
148
Q

how is convulsive status managed in hospital?

A
  • secure airway
  • give thiamine and glucose if indicated
  • IV lorazepam 2 doses
  • IV phenobarbital or phenytoin
  • Transfer to ITU
  • give midazolam, propofol or thiopental sodium to adults
  • give midazolam or thiopental sodium to children and young adults
149
Q

what are the clinical features of febrile seizures?

A
  • Febrile illness with a temperature of >38.3oC
  • Generalised tonic-clonic seizure lasting less than 15 minutes
  • No post-ictal abnormalities
150
Q

how is a febrile seizure diagnosed?

A
  • Diagnosis is clinical, but other investigations may be conducted with regards to the febrile illness:
  • Lumbar puncture to rule out meningitis
  • Viral studies
  • Blood cultures
151
Q

how should a febrile seizure be managed?

A
  • monitor and protect from injury
  • check airway and place in recovery position on cessation of seizure
  • if longer than 5 minutes, give benzodiazepine rescue medicine if recommend for the child
  • if 10 minutes, transfer to hospital
152
Q

what are the clinical features of psychogenic seizures?

A
  • Features of generalised tonic clonic seizure
  • Features suggesting NES include: duration over two minutes, gradual onset, fluctuating course, violent thrashing movements, side-to-side head movement, asynchronous movements, eyes closed and recall for period of unresponsiveness.
153
Q

what are the clinical features of an ischaemic stroke?

A
  • Vision loss or vision field defect
  • Weakness: Pure hemiparesis suggests a lacunar stroke, where other deficits suggest MCA occlusion
  • Aphasia (dominant hemisphere ischaemia)
  • Ataxia: In the absence of weakness suggests cerebellar infarction
  • Sensory loss
  • Diplopia in posterior circulation ischaemia
  • Dysarthria, particularly in cerebellar or brainstem dysfunction
  • Gaze paresis in anterior circulation strokes
  • Vertigo with posterior circulation infarction
  • Nausea and vomiting that may reflect posterior circulation ischaemia or raised ICP
  • Neck or facial pain with arterial dissection, particularly in patients with Marfan’s, or following a hairdresser appointment or osteopathic manipulation
  • Horner’s syndrome with posterior circulation
  • In an anterior circulation stroke with Horner’s syndrome, consider carotid artery dissection
  • Altered level of consciousness
154
Q

what first line investigation should be conducted in suspected stroke and what is seen?

A
  • Perform an urgent non-contrast CT head:
  • hypoattenuation of the parenchyma
  • loss of grey-white differentiation and sulcal effacement
  • hyperattenuation in an artery indicates clot in the lumen
  • primary function is to exclude haemorrhage
155
Q

what is the initial management for ischaemic stroke?

A
  • ABCDE
  • endotracheal intubation with GCS <8
  • 300mg aspirin If unsuitable for thrombosis
156
Q

what are the contraindications to thrombolysis?

A
  • Stroke or head trauma in previous 3 months
  • Any prior history of intracranial haemorrhage
  • Major surgery with 2 weeks or bleeding within 21 days
  • MI in the prior 3 months
  • Arterial or lumbar puncture within 7 days
  • Persistent systolic BP >185, diastolic >110 or requiring aggressive therapy
  • Pregnancy
  • Active bleeding or trauma
  • Thombocytopenia
  • INR >1.7
  • Elevated APTT
157
Q

what are the indications for thrombectomy in stroke?

A
  • 6 hours of symptoms onset, together with confirmed occlusion of the proximal anterior circulation demonstrated by CTA or MRA
  • within 6 to 24 hours of symptoms onset with confirmed occlusion of the proximal anterior circulation demonstrated by CTA or MRA, and there is potential to salvage brain tissue as shown by CT perfusion imaging
  • less than 3 on pre-functional modified Rankin scale
  • 5 or more on NIHSS
158
Q

What long term anti platelet therapy is given following an ischaemic stroke?

A
  • The standard treatment is clopidogrel 75mg daily
  • Modified-release dipyridamole 200 mg twice daily may be used if both clopidogrel and aspirin are contraindicated or cannot be tolerated.
  • Aspirin 75mg daily may be used if both clopidogrel and modified-release dipyridamole are contraindicated or cannot be tolerated.
  • Aspirin 75 mg daily with modified-release dipyridamole 200 mg twice daily may be used if clopidogrel cannot be tolerated.
  • Dual therapy with aspirin and clopidogrel may be initiated in secondary care for the first three months following ischaemic stroke or TIA due to severe symptomatic intracranial stenosis or for another condition such as acute coronary syndrome.
159
Q

what are the clinical features of GBS?

A
  • Progressive symmetrical muscle weakness, usually affecting the lower extremities and distal muscles first
  • Flaccid paralysis with areflexia
  • Respiratory distress
  • Paraesthesia in the hands and feet that progresses proximally
  • Back or leg pain
  • Bulbar dysfunction
  • Extra-ocular muscle weakness
160
Q

how is GBS diagnosed?

A
  • Perform nerve conduction studies: slowing of nerve conduction velocities
  • Perform a lumbar puncture: elevated CSF protein; normal or slightly raised lymphocytes
  • Perform spirometry at 6-hourly intervals: reduced vital capacity, maximal inspiratory pressure and maximal expiratory pressure
161
Q

how is GBS managed?

A
  • Start plasma exchange or IV immunoglobulin for 5 days (if there is no IgA deficiency)
  • Monitor respiratory function and intubate if needed
  • Ensure DVT prophylaxis is instituted
162
Q

what are the clinical features of MS?

A
  • Graying or blurring of vision in one eye; there may be pain on moving that eye and loss of colour discrimination, particularly reds (optic neuritis)
  • Peculiar sensory phenomena
  • Lhermitte’s sign
  • Weakness on walking that settles on rest
  • Leg cramps or jerking in the calves
  • Fatigue
  • Urinary frequency, detrusor instability and urinary retention
  • Bowel dysfunction such as constipation
  • Spasticity and increased muscle tone
  • Hyperreflexia and ankle clonus
  • Imbalance and incoordination
  • Abnormal eye movements: internuclear ophthalmoplegia (nystagmus of the abducting eye with absent adduction of the other eye)
  • Symptoms worsen with heat (Uhthoff’s phenomenon)
163
Q

how is MS diagnosed?

A
  • clinical demyelination disseminated in time and space
  • MRI brain: hyperintensities in the periventricular white matter
  • MRI spine: Demyelinating lesions in the spinal cord, particularly the cervical spinal cord; detection of alternative diagnosis, such as cervical spondylosis
164
Q

how is an acute MS relapse managed?

A
  • Offer oral methylprednisolone 0.5g daily for 5 days
  • Consider IV methylprednisolone 1g daily for 3-5 days for people in whom oral steroids have failed or are not tolerated, or who need admitting to hospital for a severe relapse or other disease monitoring.
165
Q

which DMTs are used in RRMS?

A
  • Interferon 1a

- glatiramer acetate

166
Q

which DMTs are used in active RRMS?

A
  • Interferon 1b
  • teriflunomide
  • alemtuzumab
  • ocrelizumab
167
Q

define active RRMS

A

-2 clinically significant relapses in the previous 2 years

168
Q

which DMTs are used in highly active RRMS?

A
  • fingolimod

- cladribine

169
Q

which DMTs are used in rapidly evolving RRMS?

A
  • natalizumab

- cladribine

170
Q

define highly active RRMS

A

-An unchanged/increased relapse rate, or ongoing relapses compared with the previous year despite treatment

171
Q

define rapidly evolving RRMS

A

-2 or more disabling relapses in 1 year, and one or more gadolinium-enhancing lesions on brain MRI or a significant increase in T2 lesion load compared with a previous MRI

172
Q

what are the clinical features of Huntington’s disease?

A
  • Positive family history
  • Impaired work or school performance
  • Personality change, particularly irritability or temper outbursts
  • Impulsivities
  • Chorea
  • Twitching or restlessness
  • Loss of coordination
  • Deficit in fine motor coordination
  • Slow saccadic eye movements
  • Motor impersistence
  • Impaired tandem walking
  • Concentration impairment
  • Cognitive decline
  • Changes in personal habits
  • Disinhibition or anxious behaviour
173
Q

how is Huntington’s diagnosed?

A
  • Diagnosis is clinical
  • Perform CAG repeat testing: Positive with >40 CAG repeats on 1 of the 2 alleles
  • Perform an MRI or CT scan: Caudate or striatal atrophy
174
Q

how are the features of Huntington’s diagnosed?

A
  • Prescribe tetrabenazine, sulpiride, a second generation anti-psychotic, benzodiazepines or amantadine to manage chorea without behavioural problems
  • Prescribe SSRIs for depression
  • To manage temper outbursts or irritability with carbamazepine or valproate
  • Give SSRIs or CBT with obsessive compulsive behaviours
  • To manage chorea, bradykinesia, weight loss or an acute presentation, give haloperidol, quetiapine, olanzapine or sulpiride
  • For bradykinesia without behavioural problems, give levodopa or amantadine
  • ECT can be used for refractory depression in Huntington’s
175
Q

what are the clinical features of carpal tunnel syndrome?

A
  • Numbness of the hand in the median nerve distribution (palmar aspect of the first 4 fingers) with sparing of the thenar eminence, that is worse at night
  • Weakness of the hand, particularly for rotational movements
  • Clumsiness
  • Weakness of thenar muscles (thumb abduction)
176
Q

how is carpal tunnel diagnosed?

A
  • Perform electromyography: focal slowing of conduction velocity in the median sensory nerves across the carpal tunnel; prolongation of the median distal motor latency; possible decreased amplitude of median sensory and/or motor nerves
  • Perform USS or MRI wrist: space-occupying lesion may be seen
  • Perform blood tests as appropriate if underlying cause suspected
177
Q

how is carpal tunnel managed?

A
  • Refer to an appropriate specialist if: the diagnosis is unclear, severe symptoms, reduced functional ability, recurrence following surgery, failed conservative managed or serious condition suspected
  • Optimise treatment of underlying condition and give lifestyle advice
  • Offer wrist splitting in a neutral position at night
  • Offer corticosteroid injections and follow up monthly
  • If this fails, refer for surgical decompression
178
Q

what are the clinical features of ulnar nerve compression?

A
  • clawing of the hand
  • wasting of interossei and hypothenar muscles
  • weakness of interossei and medial two lumbricals – with sensory loss in the little finger and splitting the ring finger.
179
Q

what are the clinical features of radial nerve compression?

A
  • Wrist drop

- weakness of brachioradialis and finger extension

180
Q

what are the clinical features of common peroneal nerve palsy?

A
  • foot drop
  • preserved ankle jerk
  • patch of numbness on the anterolateral border of the dorsum of the foot/lateral calf
181
Q

what are the causes of mono neuritis multiplex?

A
  • Ischaemic: vasculitis and diabetes mellitus
  • Inflammatory or immune mediated
  • Infectious
  • Drug induced: sulphonamides, PTU, hydralazine, allopurinol, cefaclor, minocycline, D-penicillamine, phenytoin, isotretinoin, methotrexate, interferons, TNF-alpha inhibitors, quinolones, leukotriene inhibitor
  • Genetics
  • Mechanical
  • Secondary to malignancy
182
Q

how is mononeuritis multiplex diagnosed?

A
  • Perform electromyography in the clinically relevant areas
  • Perform investigations to find the underlying cause
  • Peform a muscle or nerve biopsy: tissue evidence of neuropathy
183
Q

what are the clinical features of Charcot Marie tooth?

A
  • Family history of neuropathy, pes cavus or abnormal gait
  • Walking difficulties due to weakness and atrophy of the lower leg and foot
  • Pes cavus
  • Steppage gait
  • Diffuse tendon hyporeflexia or areflexia
  • Reduced muscle strength
  • Reduced sensation and sensory ataxia
  • Ankle weakness
  • Toe walking
  • Delayed motor milestones
184
Q

how is Charcot Marie tooth disease diagnosed?

A
  • Perform nerve conduction studies: conduction velocities of 15-38 m/second, reduced or absent sensory responses, and prolonged distal latencies in demyelination; reduced amplitudes and normal conduction velocities (>38m/second) in axonal loss
  • Perform genetic testing: gene mutation associated with specific CMT subtype
185
Q

how is Charcot Marie tooth disease treated?

A
  • Offer physiotherapy, exercise and occupational therapy to all patients
  • Patients should be evaluated for bracing of the feet to ensure proper alignment
  • Some patients may require orthopaedic surgery for foot deformities associated with CMT, or for secondary complications such as osteoarthritis
186
Q

what are the clinical features of neuropathic joints?

A
  • swelling
  • severe deformaties
  • instability
187
Q

what are the clinical features of chronic inflammatory demyelinating polyradiculoneuropathy?

A
  • Disease progression
  • Weakness that is typically symmetrical and involves all four limbs
  • Altered sensation
  • Decreased deep tendon reflexes
  • Incoordination
188
Q

what is seen on nerve conduction studies in chronic inflammatory demyelinating polyradiculoneuropathy?

A
  • slow conduction velocities
  • prolonged distal latencies
  • prolonged F-wave latencies
  • conduction block
189
Q

how is chronic inflammatory demyelinating polyradiculoneuropathy managed?

A
  • Observe patients with mild disease
  • Consider initial monotherapy with corticosteroids, IVIG or plasma exchange
  • Give treatment for neuropathic pain with amitriptyline, gabapentin, pregabalin or carbamazepine
  • If initial treatment fails, combine steroids with either IVIG or plasma exchange , or change which steroid is in use (methylprednisolone, dexamethasone or prednisolone)
  • alternative immunosuppressant such as ciclosporin, azathioprine, mycophenolate mofetil or rituximab
190
Q

what are the clinical features of beriberi?

A
  • Decreased sensation of the legs
  • Reduced tendon reflexes
  • Progressive muscle weakness and wasting
191
Q

how is beriberi diagnosed?

A
  • Measure erythrocyte thiamine pyrophosphate: reduced

- Perform an ABG: raised anion gap metabolic acidosis and elevated lactate

192
Q

what are the clinical features of subacute combined degeneration of the cord?

A
  • numbness and tingling of fingers and toes
  • distal sensory loss, particularly posterior column (discriminative touch, vibration and proprioception), absent ankle jerks
  • with cord involvement, exaggerated knee jerks and extensor plantars.
  • Optic atrophy and retinal haemorrhage may occur.
  • In later stages sphincter disturbance, severe generalized weakness and dementia develop.
193
Q

which drugs can cause malignant hyperpyrexia?

A
  • inhalational anaesthetics

- suxamethonium

194
Q

what are the clinical features of malignant hyperpyrexia?

A
  • Increased minute ventilation in a spontaneously breathing patient; if mechanically ventilated, there will be a substantial increase in minute ventilation required to maintain a normal end tidal CO2
  • Elevated core temperature
  • Muscular rigidity
  • Tachycardia
  • Decreased urine output
195
Q

how is malignant hyperpyrexia diagnosed?

A
  • Discontinuation of inhalational anaesthetic: partial resolution of hypercapnia, tachycardia and muscular rigidity
  • Perform a VBG: hypercapnia
  • Measure serum electrolytes: Hyperkalaemia
  • Measure creatinine kinase: >20,000 IU following suxamethonium, >10,000 without exposure
  • Perform urinalysis: positive for blood and raised urine myoglobin
196
Q

how is malignant hyperpyrexia managed?

A
  • Discontinue the triggering agent
  • Administer IV dantrolene
  • Give cold IV normal saline without potassium, uncover the patient and place cold packs in the groin, axillae, neck and around the head
  • Admit patients to ICU
  • If there is myoglobinuria or low renal output, consider bicarbonate therapy to alkalinise the urine and prevent myoglobinuria induced AKI
  • Give mannitol to increase urine output
197
Q

what are the clinical features of myasthenia gravis?

A
  • Muscle fatiguability
  • Ptosis
  • Diplopia
  • Dysphagia
  • Dysarthria
  • Facial paresis
  • Proximal limb weakness
  • Shortness of breath
198
Q

how is myasthenia gravis diagnosed?

A
  • elevated AChR or MuSK
  • repetitive nerve stimulation: 10% decline in compound muscle action potential (CMAP) amplitude between the first and fourth potential in a train of 10 stimulations of the motor nerve at 2 to 3 Hz is considered a positive response
  • edrophonium test
199
Q

how is myasthenia gravis managed?

A
  • pyridostigmine
  • further immunosuppression with prednisolone, or a steroid-sparing agent such as azathioprine, mycophenolate mofetil, tacrolimus or ciclosporin, and thymectomy if enlarged
  • If this is inadequate, consider rituximab
200
Q

how is myasthenia crisis managed?

A
  • Intubate and give mechanical ventilation if: forced vital capacity (FVC) 15 mL/kg or less (normal ≥60 mL/kg) and negative inspiratory force (NIF) 20 cm H2O or less (normal ≥70 cm H2O). Some patients may require a tracheostomy and percutaneous endoscopic gastrostomy (PEG) tube
  • Perform plasma exchange or IV immunoglobulin with high dose prednisolone
201
Q

what are the clinical features of Lambert-eaton myasthenic syndrome?

A
  • Limb weakness that begins in the proximal leg muscles and tends to improve after a few minutes of muscular contraction
  • Xerostomia
  • Waddling gait
  • Dysarthria
  • Areflexia
  • Ptosis
  • Diplopia
  • Impotence
  • Dysphagia
  • Orthostatic hypotension
202
Q

how is Lambert-eaton myasthenic syndrome diagnosed?

A
  • Perform nerve conduction studies and low frequency repetitive nerve stimulation: doubling of compound muscle action potential amplitude post-exercise
  • Perform anti P/Q voltage-gated calcium channel serology: positive
  • Perform chest CT: malignancy
203
Q

how is Lambert-eaton myasthenic syndrome managed?

A
  • Treat the underlying cause
  • Give amifampridine and pyridostigmine for symptomatic improvement
  • If symptoms do not improve, give immunomodulators such as prednisolone, azathioprine, mycophenolate mofetil or ciclosporin
  • intubate if needed
204
Q

what are the clinical features of myotonic dystrophy?

A
  • progressive distal muscle weakness
  • ptosis
  • weakness
  • thinning of the face and sternomastoids.
  • Myotonia
  • Cataracts
  • Frontal baldness
  • Cognitive impairment (mild)
  • Oesophageal dysfunction (and aspiration)
  • Cardiomyopathy and conduction defects (sudden death can occur in type 1)
  • Small pituitary fossa and hypogonadism
  • Glucose intolerance
  • Low serum IgG.
205
Q

what are the clinical features of normal pressure hydrocephalus?

A
  • Gait ataxia
  • Cognitive impairment
  • Urinary frequency, urgency or incontinence
  • Faecal incontinence
206
Q

how is NPH diagnosed?

A
  • Perform CT or MRI head:
  • mild to moderate ventricular enlargement
  • periventricular leukomalacia (i.e., damage to the white matter around the cerebral ventricles)
  • cerebral infarction
  • relative preservation of cortical gyri and sulci
  • aqueduct flow void
  • reduced diameter of the corpus callosum and decreased callosal angle
207
Q

how is NPH treated?

A

-ventriculoperitoneal shunting or endoscopic third ventriculostomy

208
Q

what are the clinical features of hydrocephalus in children?

A
  • In infants with hydrocephalus, as their skull sutures have not fused, the head circumference may be disproportionately large or show an excessive rate of growth.
  • The skull sutures separate, the anterior fontanelle bulges and the scalp veins become distended.
  • An advanced sign is fixed downward gaze or sun setting of the eyes
  • Older children will develop signs and symptoms of raised intracranial pressure.
209
Q

what are the causes of cerebral palsy?

A
  • vascular occlusion
  • cortical migration disorders or structural maldevelopment of the brain during gestation.
  • Other antenatal causes are genetic syndromes and congenital infection.
  • Hypoxic-ischaemic injury during delivery
  • Periventricular leucomalacia (PVL) secondary to ischaemia and/or severe intraventricular haemorrhage in preterm infants
  • Postnatal causes are meningitis/encephalitis/ encephalopathy, head trauma from accidental or non- accidental injury, symptomatic hypoglycaemia, hydrocephalus and hyperbilirubinaemia.
210
Q

what are the clinical features of hemiplegic spastic cerebral palsy?

A
  • unilateral involvement of the arm and leg
  • fisting of the affected hand
  • flexed arm
  • pronated forearm
  • asymmetric reaching or hand function
211
Q

what are the clinical features of quadriplegic spastic cerebral palsy?

A
  • all four limbs affected
  • opisthotonus
  • poor head control
  • low central tone
212
Q

what are the clinical features of diplegic spastic cerebral palsy?

A

-all four limbs, but the legs are affected to a much greater degree than the arms,

213
Q

what are the clinical features of dyskinetic cerebral palsy?

A
  • chorea
  • athetosis
  • dystonia
214
Q

what are the causes of chorea?

A
  • Systemic disease – thyrotoxicosis, SLE, antiphospholipid syndrome, primary polycythaemia
  • Genetic disorders – Huntington’s disease and genetic phenocopies, neuroacanthocytosis, benign hereditary chorea
  • Structural and vascular disorders affecting the basal ganglia
  • Drugs (e.g. levodopa and OC pill)
  • Post-infectious (Sydenham’s chorea), following months after streptococcal infection or as part of acute rheumatic fever
  • Pregnancy.
215
Q

what are the clinical features of discogenic back pain?

A
  • Persistent low back pain that worsens with axial loading and improves with recumbence
  • Radicular leg pain
  • Restriction in lumbar motion
  • Positive straight leg raise test
  • Neurological deficit if there is nerve root dysfunction or cauda equina syndrome
216
Q

how is discogenic back pain managed?

A
  • lumbar spine x-ray: degenerative changes (osteophytes, disc space narrowing, foraminal stenosis, endplate sclerosis, ligament calcification) may be seen
  • Perform MRI spine: signs of degeneration (decreased signal on T2-weighted images [black disc]), evaluation of disc height, presence or absence of annular tears, endplate changes
  • Perform flexion/extension spine x-rays: lumbar motion segment instability
217
Q

how should acute discogenic back pain of <3 months be managed?

A
  • Give paracetamol or an NSAID and topical analgesia
  • Advise a short period of bed rest for 2-3 days
  • Opioid analgesia can be given if pain is not controlled
  • Give a muscle relaxant such as diazepam for short term relief
  • Offer physiotherapy
218
Q

how should chronic discogenic back pain of >3 months be managed?

A
  • Continue routine pain management and refer to pain clinic
  • Offer amitriptyline for neuropathic pain
  • Offer physiotherapy
  • Refer to specialist for consideration of nerve block or decompression
219
Q

what are the clinical features of caudal equine syndrome?

A
  • Bilateral, radiating leg pain
  • Severe or progressive bilateral neurological deficit of the legs, such as major motor weakness with knee extension, ankle eversion or foot dorsiflexion
  • Difficulty initiating micturition or impaired sensation of urinary flow or urinary retention
  • Loss of sensation of rectal fullness or faecal incontinence
  • Perianal, perineal or genital sensory loss
  • Laxity of the anal sphincter
220
Q

what are the clinical features of spinal stenosis?

A
  • Insidious onset of activity related back pain
  • Leg pain when walking: neurogenic claudication that improves with rest or leaning forward
  • Stooped posture when walking: walking leant forward to flex the spine and increase the size of the spinal canal
  • Leg numbness or paraesthesia
221
Q

how is spinal stenosis diagnosed?

A
  • Perform plain spinal x-rays: degenerative changes or spondylolisthesis
  • Perform spinal MRI: compression of the neural elements and soft tissues
  • Perform EMG: increased F latency values
222
Q

how is spinal stenosis managed?

A
  • If there is significant acute neurological deficit, perform surgical decompression
  • Otherwise, give standard analgesia and advise a short period of bed rest until the acute episode settle
  • If anti-inflammatory drugs and paracetamol fail, give a short course of steroids
  • For chronic symptoms, advise standard analgesia and chronic pain agents such as amitriptyline or gabapentin
  • decompressive laminectomy after 3 months
223
Q

what are the clinical features of neural tube defects?

A
  • Maternal risk factors, increased triple or quadruple test markers or USS abnormality
  • Closed spina bifida lesion: asymmetrical gluteal fold or dimple, haemangioma, hairy patch or other cutaneous markings
  • Abnormal urinary voiding
  • Leakage of meconium or stool
  • Absence of rectal tone
  • Asymmetry of spontaneous arm and leg movement
  • Difficulty with changing nappies or dressing due to spasticity
  • Abnormal muscle tone and bulk in arms and legs
  • Decreased sensation
  • Clubfoot
  • Vertical talus
  • Hip and knee flexion contractures
224
Q

how are neural tube defects diagnosed?

A
  • antenatal

- spinal ultrasound; tethering, diastomyelia, hydromyelia or syringomyelia

225
Q

what are the clinical features of essential tremor?

A
  • Bilateral upper limb action tremor, with the absence of other neurology
  • Difficulties with fine motor tasks
  • Abatement of tremor after consumption of alcohol, benzodiazepines, barbiturates or gabapentin
  • Head or voice tremor
226
Q

how is essential tremor managed?

A
  • Offer propranolol, primidone or gabapentin to improve functioning
  • Treatments for refractory essential tremor is deep brain stimulation, focused US thalamotomy and gamma knife thalamotomy
227
Q

what are the clinical features of spinal cord compression?

A
  • Patients with trauma, disc disease or malignancy
  • Back pain
  • Numbness or paraesthesia
  • Weakness or paralysis: loss of fine finger movements, difficulty walking
  • Bladder or bowel dysfunction are seen in long standing compression and cauda equina
  • Hyper-reflexia
  • Loss of tone below the level of an injury
  • Hypotension and bradycardia if associated with neurogenic shock
228
Q

how is spinal cord compression diagnosed?

A

-Perform MRI spine: disc displacement; epidural enhancement; mass effect; T2 cord signal

229
Q

how is spinal cord compression managed?

A
  • If there is acute spinal cord injury, use an ABCDE approach and immobilise the spine and perform decompressive or stabilisation surgery
  • Give intravenous corticosteroids to reduce oedema of the spinal cord
  • If a non-traumatic cause, perform decompressive laminectomy
  • In malignant spinal cord compression, give steroids to reduce oedema and perform surgery or radiation as needed
  • If there is an epidural abscess, give vancomycin, metronidazole and cefotaxime with surgical drainage
230
Q

what are the clinical features of lumbar radiculopathy?

A
  • Unilateral leg pain radiating to below the knee to the foot or toes
  • Low back pain
  • Numbness, paraesthesia and muscle weakness in the distribution of the L5 dermatome
  • Positive straight leg raise
231
Q

how is lumbar radiculopathy managed?

A

-Offer self-management advice and analgesia such as NSAIDs (with gastroprotection), or if contraindicated offer co-codamol

  • For patients at a higher risk of a poor outcome:
  • –Offer referral for a group exercise programme
  • –Consider referral to physiotherapy
  • consider offering treatment for neuropathic pain
  • If there is progressive, persistent or severe neurological deficit, refer urgently to neurosurgery
232
Q

what are the symptoms of cerebellar dysfunction?

A
  • Slurring of speech
  • Swallowing difficulties
  • Oscillopsia
  • Clumsiness
  • Action tremor
  • Loss of precision of fine motor skills
  • Unsteadiness when walking that is worse in the dark
  • Stumbles/falls
233
Q

what are the signs of cerebellar dysfunction?

A
  • nystagmus
  • Dysarthria
  • Action tremor
  • Dysdiadochokinaesia
  • Truncal ataxia
  • Limb ataxia
  • Gait ataxia
234
Q

what are the causes of coma?

A
  • vascular
  • infection
  • TBI, brain tumour, syncope
  • electrolyte disorders
  • endocrine disorders
  • inborn errors of metabolism
  • toxic
235
Q

what are the clinical features of central sleep apnoea?

A
  • Insomnia
  • Poor concentration and attention span
  • Observed periodic breathing or cessation of breathing or snoring during sleep
  • Transient dyspnoea that awakens from sleep
  • Headaches on arising
236
Q

how is central sleep apnoea diagnosed?

A

-Polysomnography >5 central apnoeas or hypopnoeas per hour of sleep and the total number of central apnoeas and/or central hypopnoeas is >50% of the total number of apnoeas and hypopnoeas

237
Q

how is central sleep apnoea managed?

A
  • CPAP

- supplemental oxygen

238
Q

what are the clinical features of a cerebral AVM?

A
  • Features of intracerebral haemorrhage
  • Seizures
  • Headaches
239
Q

how is cerebral AVM diagnosed?

A
  • Perform CT brain: reveals intracerebral haemorrhage; identifies AVM by calcification and isointense or slightly hyperintense vessels
  • Perform MRI brain detects AVMs ± haemorrhage, and thrombosed vessels
  • Perform brain angiogram: early venous filling (indicating arteriovenous shunting) during arterial phase
240
Q

how is a cerebral AVM managed?

A
  • In a non-ruptured AVM, surgical resection or staged embolisation can be performed (for larger AVM)
  • Stereotactic radiosurgery is possible in inaccessible AVMs
241
Q

what are the clinical features of tuberous sclerosis?

A
  • Epilepsy
  • Cardiac rhabdomyoma
  • Renal angiomyolipomas
  • Lymphangioleiomyomatosis of the lung
  • Cerebral subependymal calcified nodules
  • Giant cell astrocytoma
  • Facial angiofibromas
  • Cephalic plaque
  • Non-traumatic ungual or periungual fibromas
  • Hypomelanocytic macules
  • Shagreen patches
  • Numerous dental enamel pits
  • Gingival fibromas
  • Retinal nodular hamartomas
  • Cognitive impairment
  • Depigmented ‘ash leaf’-shaped patches which fluoresce under ultraviolet light
242
Q

what are the clinical features of transverse myelitis?

A
  • Progressive weakness of the extremities
  • Paraesthesias or sensory loss, beginning in the distal limbs and settling at or a few levels below the spinal lesion
  • Urinary disturbance and bowel symptoms
  • Paroxysmal tonic spasms
  • Upper motor neurone signs
  • Sensory level: reduced pain or temperature sensation below the level of the lesion
  • Back pain
243
Q

how is transverse myelitis managed?

A
  • If there is acute neurological deficit, give corticosteroids, plasma exchange and supportive care
  • If the patient is found to have idiopathic TM, observe
244
Q

what are the clinical features of raised ICP?

A
  • Headache (worse on coughing, leaning forwards), vomiting
  • Altered GCS: drowsiness, listlessness, irritability, coma
  • History of trauma
  • Low heart rate and high blood pressure; Cheyne-Stokes Response
  • Pupil changes: constriction at first, later dilation – do not mask by using tropicamide to dilate to aid fundoscopy
  • Low visual acuity; peripheral visual field loss
  • Papilloedema is an unreliable sign, but venous pulsation at the disc may be absent
245
Q

how is raised ICP managed?

A
  • Correct hypotension, maintain mean arterial pressure >90mmHg and treat seizures as necessary
  • Elevate the head of the bed to 30-40o
  • If the patient is intubated, hyperventilate to a PaCO2 of 3.5-4kPa).
  • Give 20% mannitol 0.25-5g/kg IV over 10-20 minutes and follow serum osmolality, aiming for 300mosmol/kg, and not exceeding 310
  • Give dexamethasone to reduce oedema surrounding tumours
  • Restrict fluid to <1.5L/day
  • Monitor the patient and consider ICP monitoring
  • Treat hyperglycaemia and hyponatraemia as necessary
  • Treat the underlying cause
246
Q

what are the signs of a 3rd nerve palsy?

A
  • Unilateral complete ptosis (levator weakness)
  • Eye deviated down and out (unopposed lateral rectus and superior oblique)
  • A fixed and dilated pupil.
247
Q

what are the clinical features of a 4th nerve palsy?

A
  • torsional diplopia (two objects at an angle) when attempting to look down (e.g. descending stairs)
  • the head is tilted away from that side.
248
Q

what are the clinical features of a 6th nerve palsy?

A

-horizontal diplopia

249
Q

what are the clinical features of a 5th nerve palsy?

A
  • unilateral sensory loss on the face
  • scalp anterior to the vertex, anterior two-thirds of the tongue and buccal mucosa
  • the jaw deviates to that side as the mouth opens (motor fibres).
  • Diminution of the corneal reflex is an early and sometimes isolated sign of a Vth nerve
250
Q

what are the clinical features of Bell’s palsy?

A
  • Unilateral facial weakness
  • Keratoconjunctivitis sicca (dry eye)
  • Post-auricular pain and otalgia
  • Facial synkinesis
  • Hyperacusis
251
Q

how is Bell’s palsy managed?

A
  • Advise the patient to keep the affected eye lubricated with lubricating eye drops and tape the eye shut at night
  • For people presenting within 72 hours of the onset of symptoms, consider prednisolone
252
Q

what are the clinical features of myelopathy?

A
  • Motor weakness
  • Loss of fine motor co-ordination
  • Spasticity
  • Paraesthesia, numbness and dysaesthesia
  • Hyper-reflexia
253
Q

how is myelopathy diagnosed?

A
  • Perform MRI: Vertebral body or spinal cord lesions

- Perform EMG: Decreased spinal cord conduction

254
Q

how is myelopathy managed?

A
  • If there is evidence of a progressive neurological deficit, the patient should be urgently assessed and there should be surgical decompression
  • If there is autonomic dysreflexia, treat the cause of the excessive autonomic response e.g. treat constipation or urinary retention
  • If symptoms persist despite treatment, give nifedipine or GTN to lower the BP
  • If the neurological status is stable, offer physiotherapy and mobilisation, with supportive care including bladder and bowel management and pain management with anti-neuropathic agents
255
Q

what are the clinical features of cavernous sinus thrombosis?

A
  • Rapid onset of symptoms
  • Headache
  • Fever
  • Periorbital oedema
  • Chemosis and proptosis
  • Lateral gaze palsy
  • Ophthalmoplegia
  • Sepsis
  • Ptosis and mydriasis
  • Decreased corneal reflex
  • Hypo or hyperaesthesia in the distribution of V1 and V2
256
Q

how is cavernous sinus thrombosis diagnosed?

A
  • expansion of the cavernous sinuses
  • convex bowing of lateral walls
  • increased dural enhancement
  • sphenoid sinus pathology may be present
257
Q

how is septic cavernous sinus thrombosis managed?

A

-vancomycin, ceftriaxone and metronidazole

258
Q

how is cavernous sinus thrombosis managed?

A

-Offer people diagnosed with cerebral venous sinus thrombosis full dose anticoagulation (heparin then warfarin with an INR of 2 to 3)

259
Q

what are the symptoms of cervical radiculopathy?

A
  • Pain in the neck, shoulder and/or arm that approximates to that of a dermatome.
  • It is usually unilateral, but may be bilateral.
  • The pain may be severe enough to wake the person at night.
  • Sensory symptoms, such as absent or altered sensation (for example, shooting pains, numbness, and hyperaesthesia).
  • Sensory symptoms are more common than motor symptoms.
  • Motor symptoms, such as muscle weakness.
  • Gradual onset, although it may be abrupt.
  • Retro-orbital and temporal pain suggest referral from the upper cervical levels (C1 to C3)
260
Q

what are the signs of cervical radiculopathy?

A
  • Postural asymmetry
  • If the asymmetry is long-standing, muscle wasting may be present.
  • Neck movements
  • Dural irritation
  • Neurological problems — for example, upper limb weakness, paraesthesia, dermatomal sensory or motor deficit, or diminished tendon reflexes at the appropriate level.
  • Atypical signs of cervical radiculopathy include: deltoid weakness, scapular winging, weakness of the intrinsic muscles of the hand, chest or deep breast pain, and headaches.
261
Q

how is cervical radiculopathy managed?

A
  • Provide conservative management
  • Encourage activity
  • Advice that a firm pillow may provide comfort at night
  • Offer NSAIDs, paracetamol or codeine
  • Consider offering amitriptyline, duloxetine, pregabalin or gabapentin and muscle relaxants
  • if more than 6 weeks, confirm diagnosis with MRI and consider epidural or surgery
262
Q

how is neuropathic pain managed?

A
  • Offer a choice of amitriptyline, duloxetine, gabapentin or pregabalin as initial treatment for neuropathic pain
  • Consider capsaicin cream for people with localised neuropathic pain
  • refer to pain service
263
Q

how is trigeminal neuralgia managed?

A
  • carbamazepine

- microvascular decompression

264
Q

what are the clinical features of Duchenne muscular dystrophy?

A
  • Imbalance of lower limb strength
  • Lower extremity musculotendinous contractures
  • Delayed motor milestones
  • Calf hypertrophy
  • Ambulation difficulty and falls.
  • Diminished muscle tone and deep tendon reflexes
  • Normal sensation
  • Gowers’ sign: patient climbs up his legs
  • Toe walking
265
Q

how is Duchenne muscular dystrophy diagnosed?

A
  • Measure serum creatinine kinase: 50 to 100 times normal
  • Perform genetic testing: Xp21 mutation
  • Perform EMG: myopathic reading with fast firing, short duration but polyphasic and decreased amplitude motor units with early recruitment in the affected muscles
  • Perform muscle biopsy: absence of dystrophin with Duchenne muscular dystrophy; diminished quantity or quality of dystrophin with Becker muscular dystrophy
266
Q

how is muscular dystrophy managed?

A
  • Give prednisolone therapy to improve muscle strength and function
  • Provide physiotherapy, exercise and psychological support
  • Perform surgery for contractures
  • Give carvedilol and lisinopril for cardioprotection from 10 years old
  • As vital capacity diminishes, give intermittent positive pressure ventilation and consider indwelling gastrostomy to maximise nutrition
  • Perform surgery for scoliosis
267
Q

what are the clinical features of poliomyelitis?

A
  • Fever
  • Sore throat
  • Myalgia
  • Meningeal irritation
  • Decreased tone and motor function
  • Decreased tendon reflexes
  • Muscle atrophy
  • No sensory changes: distinguishes from GBS
268
Q

how is poliomyelitis managed?

A
  • Provide supportive care with rehydration and neurological monitoring
  • Offer physiotherapy with mobilisation
  • If there is respiratory paralysis, intubate and ventilate
269
Q

what are the clinical features of cervical spondylosis?

A
  • Spontaneous onset of neck pain
  • Cervical muscle pain and spasm
  • Headaches or occipital pain
  • Weakness or numbness and radiating arm pain with associated radiculopathy
270
Q

how is cervical spondylosis managed?

A
  • Offer physiotherapy and NSAIDs for axial neck pain
  • Offer muscle relaxants if there is cervical muscle spasm
  • Consider corticosteroid injections into the joint
271
Q

what signs are required for a diagnosis of neurofibromatosis type 1?

A
  • Six or more café-au-lait spots>5mm in size before puberty, >15 mm after puberty
  • Axillary freckling
  • Neurofibromas
  • Compromised vision due to optic gliomas
  • Iris Lisch nodules
  • Sphenoid wing dysplasia
272
Q

what are the clinical features of neurofibrotmatosis type 2?

A
  • Bilateral acoustic neuromata
  • deafness
  • cerebellopontine angle syndrome with a facial (VIIth) nerve paresis and cerebellar ataxia.
273
Q

what are the clinical features of a brain abscess?

A
  • Meningism
  • Headache
  • Cranial nerve palsy: 3rd and 6th nerve
  • Positive Kernig or Brudzinski sign
  • Fever
  • Neurological findings
  • In children: increased head circumference and bulging fontanelle
274
Q

what is seen on MRI head in brain abscess?

A

-Ring-enhancing lesion

275
Q

what are the indications for CT head within 1 hour in an under 16 year old with a head injury?

A
  • Suspicion of non-accidental injury
  • Post-traumatic seizure with no history of epilepsy
  • GCS <14, or if under 1 GCS <15
  • GCS <15 after 2 hours
  • Suspected open or depressed skull fracture or tense fontanelle
  • Any sign of basal skull fracture (haemotypanum, panda eyes, CSF leakage from the ear or nose, Battle’s sign/bruising over the mastoid)
  • Focal neurology
  • Bruise, swelling or laceteration >5cm on the head if under 1
  • More than 5 minutes loss of consciousness
  • Abnormal drowsiness
  • Three or more discrete episodes of vomiting
  • Dangerous mechanism of injury
  • Amnesia
276
Q

what are the indications for CT within 1 hour in an adult with head injury?

A
  • GCS <13 or <15 after 2 hours
  • Suspected skull fracture or any sign of basal skull fracture (haemotypanum, panda eyes, CSF leakage from the ear or nose, Battle’s sign/bruising over the mastoid)
  • Post-traumatic seizure
  • Focal neurological deficit
  • More than 1 episode of vomiting
277
Q

what are the indications for CT within 8 hours in an adult with head injury?

A
  • 65 years or older
  • History of bleeding or clotting disorders
  • Dangerous mechanism of injury
  • More than 30 minutes of retrograde amnesia of events immediately before the head injury
  • anticoagulant treatment
278
Q

when should the range of neck movement be assessed in a patient with head injury?

A
  • Was involved in a simple rear-end motor vehicle collision
  • Is comfortable in a sitting position
  • Has been ambulatory
  • Has no midline c-spine tenderness
  • Presents with delayed onset of neck pain
279
Q

when should c-spine x-rays be done in an under 16 year old with a head injury?

A
  • child cannot actively rotate their neck 45 degrees to the left and right on assessment of the neck
  • Dangerous mechanism of injury e.g. fall from height of more than 1 metre, axial load to the head, high speed crash, rolled motor vehicle, ejection from motor vehicle, accident involving motorised recreational vehicles or bicycle collision
  • Safe assessment of the range of movement of the neck is not possible
280
Q

when should c-spine x-rays be done in an over 16 year old with a head injury?

A
  • It is not safe to assess range of neck movement

- Safe assessment of neck movement shows that the patient cannot actively rotate their neck 45 degrees

281
Q

when should c-spine CT be done in an under 16 year old with a head injury?

A
  • GCS <13
  • The patient is intubated
  • Focal peripheral neurology
  • Paraesthesia in the upper or lower limbs
  • A C-spine injury diagnosis is needed prior to surgery
  • The patient is having other body areas scanned
  • There is strong clinical suspicion despite normal x-rays or there are significant bony injuries on x-ray
282
Q

when should c-spine CT be done in an over 16 year old with a head injury?

A
  • GCS less than 13 on initial assessment.
  • The patient has been intubated.
  • Plain X-rays are technically inadequate
  • Plain X-rays are suspicious or definitely abnormal.
  • A definitive diagnosis of cervical spine injury is needed urgently (for example, before surgery).
  • The patient is having other body areas scanned for head injury or multi-region trauma.
  • The patient is alert and stable, there is clinical suspicion of cervical spine injury and any of the following apply: over 65, dangerous mechanism, focal neurology, paraesthesia in limbs
283
Q

which patients should be admitted to hospital following a head injury?

A
  • Patients with new, clinically significant abnormalities on imaging.
  • Patients whose GCS has not returned to 15 after imaging, regardless of the imaging results.
  • When a patient has indications for CT scanning but this cannot be done within the appropriate period.
  • Continuing worrying signs (for example, persistent vomiting, severe headaches)
  • Other sources of concern to the clinician (for example, drug or alcohol intoxication, other injuries, shock, suspected non-accidental injury, meningism, cerebrospinal fluid leak).
284
Q

what are the indications for intubation following a head injury?

A
  • Coma – not obeying commands, not speaking, not eye opening (that is, GCS 8 or less).
  • Loss of protective laryngeal reflexes.
  • Ventilatory insufficiency as judged by blood gases: hypoxaemia (PaO2 < 13 kPa on oxygen) or hypercarbia (PaCO2 > 6 kPa).
  • Spontaneous hyperventilation causing PaCO2 < 4 kPa.
  • Irregular respirations.
285
Q

what are the clinical features of a spinal abscess?

A
  • Fever
  • Spinal pain or tenderness
  • Weakness of extremities
  • Paralysis
  • Sensory disturbance
  • Abnormal reflexes
286
Q

how is a spinal abscess diagnosed?

A

-Gadolinium enhanced diffusion weighted MRI spine: infection in epidural space

287
Q

what are the adverse effects of dopaminergic drugs?

A
  • Nausea
  • Drowsiness
  • Confusion
  • Hallucinations
  • Hypotension
  • Wearing off effect where adverse effects worsen towards the end of the dosage interval.
288
Q

in which patients should dopaminergic drugs be used cautiously?

A
  • Caution in the elderly
  • Caution with existing cognitive or psychiatric disease due to confusion and hallucinations
  • Caution with cardiovascular disease due to hypotension.
289
Q

with which drugs do dopaminergic agents interact?

A

-Antipsychotics and metoclopramide because their effects on dopamine receptors are contradictory.

290
Q

what are the adverse effects of strong opioids?

A
  • Respiratory depression due to reduced respiratory drive
  • Neurological depression
  • Nausea and vomiting by activating CTZ
  • Pupillary constrictor due to stimulation of Edinger-Westphal nucleus
  • Constipation due to activation of mu receptors in the gut
  • Histamine release from mast cells causes itching, hypotension and bronchoconstriction
  • Tolerance and dependence
  • Withdrawal reaction characterised by pain, breathlessness and pupillary dilation.
291
Q

in which patients should strong opioids be used cautiously?

A
  • Avoid in biliary colic due to spasm of sphincter of Oddi which may worsen pain;
  • Caution in hepatic failure
  • Caution in renal impairments
  • Caution in the elderly
  • Avoid in respiratory failure except under senior guidance.
292
Q

with which drugs do strong opioids interact?

A

Administration with sedating drugs require close monitoring.

293
Q

what are the adverse effects of naloxone?

A

-Opioid withdrawal reaction characterised by pain, anxiety, nausea and vomiting, dilated pupils, cold dry skin and piloerection.

294
Q

what are the adverse effects of weak opioids?

A
  • Nausea
  • Constipation (tramadol causes less)
  • Dizziness
  • Drowsiness
  • Neurological and respiratory depression in overdose
  • Anaphylactic reaction if given intravenously
295
Q

in which patients should weak opioids be used cautiously?

A
  • Avoid tramadol in patients with epilepsy as it lowers seizure threshold
  • Caution in significant respiratory disease
  • Caution in renal impairment
  • Caution in hepatic impairment
  • Caution in the elderly
296
Q

with which drugs do weak opioids interact?

A
  • Increased sedative effect with other sedating drugs such as antipsychotics, benzodiazepines
  • Increased risk of seizures with other drugs that lower seizure threshold e.g. SSRIs, TCAs.
297
Q

what are the adverse effects of paracetamol?

A

-liver failure in excess

298
Q

in which patients should paracetamol be used cautiously?

A
  • Avoid in chronic excessive alcohol use due to increased NAPQI production;
  • Avoid in malnutrition and severe hepatic impairment due to reduced glutathione stores.
299
Q

with which other drugs does paracetamol interact?

A

-CP450 inducers such as phenytoin and carbamazepine increase rate of NAPQI production and increase risk of liver toxicity.

300
Q

what are the adverse effects of carbamazepine?

A
  • GI upset including nausea and vomiting
  • Neurological effects including dizziness and ataxia
  • Hypersensitivity manifests as a maculopapular skin rash
  • Antiepileptic hypersensitivity syndrome manifests as severe skin reactions (Stevens-Johnson syndrome, toxic epidermal necrolysis), fever and lymphadenopathy, and systemic toxicity
  • Oedema
  • Hyponatraemia.
301
Q

in which patients should carbamazepine be used cautiously?

A
  • Caution in pregnancy due to neural tube defects, cardiac and urinary abnormalities, and cleft palate
  • Avoid with prior antiepileptic hypersensitivity syndrome;
  • Caution with hepatic, renal or cardiac disease due to increased risk of toxicity.
302
Q

with which drugs does carbamazepine interact?

A
  • CYP450 inducer so it reduced concentration of warfarin, decreases its anticoagulant effect and increases INR. Also reduces efficacy of oestrogens and progestogens.
  • Reduced plasma concentration with CYP450 inhibitors such as macrolides.
  • Complex interactions with other antiepileptic drugs
  • Efficacy reduced by drugs that lower seizure threshold (e.g. SSRIs, TCAs, antipsychotics, tramadol).
303
Q

what are the adverse effects of gabapentin and pregabalin?

A
  • Drowsiness
  • Dizziness
  • Ataxia.
304
Q

in which patients should gabapentin and pregabalin be used cautiously?

A

-renal impairment

305
Q

with which drugs do gabapentin and pregabalin interact?

A

-Increased sedative effect with other sedating drugs e.g. benzodiazepines.

306
Q

what are the adverse effects of lamotrigine?

A
  • Blurred vision
  • Aggression
  • Agitation
  • Stevens-Johnson syndrome
  • Toxic epidermal necrolysis
  • Disseminated intravascular coagulation
  • Bone marrow failure.
307
Q

in which patients should lamotrigine be used cautiously?

A
  • Avoid in pregnancy
  • Avoid in patients with known hypersensitivity to lamotrigine
  • Discontinue if rash or serious skin reaction occurs
  • Caution in hepatic or renal impairment;
  • Caution in patients myoclonic seizures.
308
Q

with which drugs does lamotrigine interact?

A
  • Induces CYP450 enzymes so reduces plasma concentration and efficacy of drugs that are metabolised by P450 enzymes, including warfarin, oestrogens and progestogens
  • CYP450 inhibitors (e.g. macrolide) increase its concentration and adverse effects
  • Complex interactions with other antiepileptic drugs; Efficacy reduced by drugs that lower seizure threshold (e.g. SSRIs, TCAs, antipsychotics, tramadol).
309
Q

what are the adverse effects of levetiracetam?

A
  • Nasopharyngitis
  • Aggression
  • Agitation
  • Dizziness and drowsiness
  • Stevens- Johnson syndrome.
310
Q

in which patients should levetiracetam be used cautiously?

A
  • Avoid in pregnancy and breastfeeding

- Caution in hepatic and renal impairment.

311
Q

with which drugs does levetiracetam interact?

A

-Efficacy reduced by drugs that lower seizure threshold (e.g. SSRIs, TCAs, antipsychotics, tramadol).

312
Q

what are the adverse effects of sodium valproate?

A
  • GI upset including nausea and diarrhoea
  • Neurological and psychiatric effects including tremor, ataxia and behaviour disturbances
  • Thrombocytopenia
  • Transient increase in liver enzymes
  • Hair loss
  • Severe liver injury
  • Pancreatitis
  • Bone marrow failure
  • Antiepileptic hypersensitivity syndrome.
313
Q

in which patients should sodium valproate be used cautiously?

A
  • Avoid in women of child bearing age
  • Avoid in first trimester of pregnancy
  • Avoid in hepatic impairment
  • Caution in severe renal impairment.
314
Q

with which other drugs does sodium valproate interact?

A
  • CYP450 inhibitor so it increases concentration of warfarin, increasing its anticoagulant effect and decreases INR. Also increases concentration of oestrogens and progestogens.
  • Reduced concentration by CYP450 inducers such as phenytoin and carbamazepine.
  • Increased adverse effects with CYP450 inhibitors such as macrolides.
  • Efficacy reduced by drugs that lower seizure threshold (e.g. SSRIs, TCAs, antipsychotics, tramadol).
315
Q

what are the adverse effects of benzodiazepines?

A
  • Drowsiness
  • Sedation
  • Coma
  • Airway obstruction and death in overdose
  • Dependence
  • Withdrawal reaction.
316
Q

in which patients should benzodiazepines be used cautiously?

A
  • Avoid with respiratory impairment
  • Avoid with neuromuscular disease such as myasthenia gravis
  • Avoid in liver failure as they may precipitate hepatic encephalopathy, however if essential lorazepam is best choice as it depends less on liver for its elimination.
317
Q

with which other drugs do benzodiazepines interact?

A
  • Increased sedation with other sedating drugs including alcohol and opioids
  • Increased effects with CYP450 inhibitors including amiodarone, diltiazem, macrolides and fluconazole.
318
Q

what are the adverse effects of phenytoin?

A
  • P: P450 Interactions
  • H: Hirsutism
  • E: Enlarged gums
  • N: Nystagmus
  • Y: Yellow-browning of skin
  • T: Teratogenic / Toxicity in overdose (cardiovascular collapse and respiratory depression)
  • O: Osteomalacia by inducing vitamin D metabolism.
  • I: Interferes with folate metabolism leading to anaemia.
  • N: Neuropathy including vertigo and ataxia
319
Q

in which patients should phenytoin be used cautiously?

A
  • Avoid in patients of Han Chinese or Thai origin due to increased risk of Stevens- Johnson syndrome
  • Caution in patients undergoing enteral feeding
  • Caution in hepatic impairment.
320
Q

with which drugs does phenytoin interact?

A
  • Adverse effects are worsened by amiodarone, diltiazem and fluconazole
  • Complex interactions with other antiepileptic drugs
  • Efficacy reduced by drugs that lower seizure threshold (e.g. SSRIs, TCAs, antipsychotics, tramadol).
321
Q

what are the adverse effects of memantine?

A
  • Dizziness
  • Drowsiness
  • Confusion
  • Thrombosis.
322
Q

in which patients should memantine be used cautiously?

A
  • Avoid in severe hepatic impairment
  • Caution in cardiac disease
  • Caution with a history of convulsions
323
Q

with which drugs does memantine interact?

A

Increased risk of CNS toxicity with amantadine and ketamine.

324
Q

what are the adverse effects of hypnotics?

A
  • Daytime sleepiness
  • Rebound insomnia when stopped
  • Nightmares
  • Amnesia
  • Zopiclone causes taste disturbance
  • Zolpidem causes GI upset
  • Dependence and withdrawal symptoms beyond four weeks characterise by headache, muscle pains and anxiety
  • Drowsiness, coma and respiratory depression in overdose.
325
Q

In which patients should hypnotics be used cautiously?

A
  • Avoid in obstructive sleep apnoea
  • Avoid in respiratory muscle weakness
  • Avoid in respiratory depression
  • Caution in the elderly.
326
Q

which drugs do hypnotics interact with?

A
  • Enhances sedative effects of antihistamines and benzodiazepines
  • P450 inhibitors (macrolides) enhance sedation
  • P450 inducers impair sedation.

FINALS (18 decks)

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