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Clinical Medicine > Neurology > Flashcards

Neurology Flashcards

1
Q

Virchow’s Triad

A

Factors which increase risk of thrombosis: Hypercoagulable state, vascular injury, circulatory status

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2
Q

Most common site of Cavernous Venous Sinus Thrombosis

A

Transverse > Sagittal > sigmoid

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3
Q

Cavernous Venous Sinus Thrombosis is most commonly a complication of:

A

Acute sinusitis

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4
Q

Risk Factors for Cavernous Venous Sinus Thrombosis

A 
Female > male (3:1)
Under 50 years
Antiphospholipid antibodies (history of miscarriage)
Cirrhosis 
Pregnancy
IBD
Otitis media
Combined OCP
Dehydration 
SLE (PMH or FH)
Factor V Leiden
Sarcoidosis 
History of tobacco and ecstasy use 
History of sinusitis, facial infection or periorbital infection
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5
Q

Most common symptom of Cavernous Venous Sinus Thrombosis

A

Headache (90%) - progressive, constant, diffuse, worse on lying down

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6
Q

Signs of Cavernous Venous Sinus Thrombosis

A

Signs of raised ICP

Eye Changes: Proptosis, Chemosis - distension of orbital veins

Motor: Ophthalmoplegia, Hyperreflexia, Aphasia, Hemianopia, Hemiparesis

Sensory: Ophthalmic/Maxillary paraesthesia

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7
Q

Proptosis

A

Anteriorly displaced orbit

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8
Q

Cushing Reflex

A

HTN and slow pulse indicating severe raised ICP and risk of herniation

May also have wide pulse pressure and irregular respiration.

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9
Q

Differentials for Cavernous Venous Sinus Thrombosis

A

Space occupying lesion:
Tumor abscess
Intracranial haemorrhage
Arterial stroke
Idiopathic intracranial hypertension (IIH) - once CVST has been excluded
Meningitis (fever, headache, vomiting, nuchal rigidity)
HIV-associated opportunistic infections e.g. CMV encephalitis
Migraine
Encephalitis esp. Herpes Simplex

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10
Q

Empty delta sign

A

Dense white triangle of impaired filling seen in Cavernous Venous Sinus Thrombosis on contrast-enhanced CT

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11
Q

Management of Cavernous Venous Sinus Thrombosis

A

Initially, vancomycin and 3rd generation cephalosporin (Ceftriaxone)
Anticoagulation

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12
Q

Anticoagulation in Cavernous Venous Sinus Thrombosis

A

Start Hep/LMWH at Day 1. Start Warfarin at Day 5. Stop Hep/LMWH when INR > 2.

3 months if secondary to transient risk factor e.g. Pregnancy
6-12 months if idiopathic or secondary to mild thrombophilia
Indefinitely if recurrent CVST or severe thrombophilia

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13
Q

Epidural Abscesses arise from

A

osteomyelitis or TB of vertebral column
Infection of a traumatic epidural haematoma
Infection of air sinuses

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14
Q

Subdural Abscesses arise from

A

Air sinuses

Middle ear

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15
Q

Presentation of Epidural Abscess

A

Fever
Spinal pain or tenderness - increased with weight-bearing, not relieved by rest

Often IVDU, immunocompromised, Hx of spinal surgery/trauma

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16
Q

Presentation of Subdural Abscesses

A

Neurological deficit or raised ICP

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17
Q

Management of Epidural Vs Subdural Abscesses

A

Epidural: Triple Antibiotic regimen, Vancomycin + Metronidazole, Ceftaxime

Subdural - evacuation + IV antibiotics

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18
Q

Intracerebral Abscess arise from what types of infection?

  • Sites
  • Trauma/Surgical
A 
Commonly spread from:
Adjacent Air sinuses
Middle Ear
Bloodstream from Bronchiectasis or lung abscess 
Bacterial endocarditis 
Neurosurgical procedures 
Open head injuries
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19
Q

Risk Factors for Brain Abscess

A 
Sinusitis
Otitis media
Recent dental procedure or infection
Recent neurosurgery
Congenital Heart Disease
Endocarditis
DM
Immunocompromised
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20
Q

Presentation for Brain Abscess

A

Headache
Symptoms of Infection
Focal neurological deficits due to destruction of brain tissue
Seizures
Raised ICP - bulging fontanelles, papilloedema
CN III or VI palsy
Positive Kernig or Brudzinski sign

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21
Q

MRI findings of Brain Abscess

A

Ring enhancing pattern with cerebral oedema (vascular leakage)

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22
Q

Management of Brain Abscess

A

All patients:
Antibiotics: vancomycin + metronidazole/clindamycin + cephalosporin
Anticonvulsant prophylaxis: phenytoin, carbamazepine, valproate, levetiracetam
Corticosteroids = rapid reduction in vasogenic oedema (avoid if stable due to suppressed immune response)

Drainage or surgical excision

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23
Q

Presentation of Bacterial Meningitis

A

Initial symptoms :
Severe headache
Fever
Stiff neck (signs right)

Other features:
Leg pains 
Cold hands and feet 
Abnormal skin colour 
Photophobia 
N&V
Late signs:
Low GCS or coma 
Seizures and focal neurological signs 
Petechial rash - non blanching 
Shock (disseminated intravascular coagulation, prolonged capillary refill, hypotension)
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24
Q

Bacterial CSF

A

Cloudy
Low glucose
High protein
WCC - polymorphs

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25
Q

Viral CSF

A

Clear or cloudy
Low or normal glucose
Normal or raised protein
WCC - lymphocytes

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26
Q

TB CSF

A

Cloudy
Very low glucose
High protein
WCC - lymphocytes

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27
Q

Empirical antibiotics in bacterial meningitis (< 3 months)

A

IV amoxicillin + cefotaxime

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28
Q

Empirical antibiotics in bacterial meningitis (> 3 months)

A

IV ceftriaxone

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29
Q

Steroid treatment in bacterial meningitis:

  • Indications
  • Regimen
  • Effect
A

Dexamethasone

Indicated if > 1 month and H.influenzae
Before or within 4 hours of first dose Abx
Reduces rate of hearing loss and neurological sequelae.

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30
Q

Empirical antibiotics in adults with bacterial meningitis

A

< 50 years = IV cefotaxime

> 50 years = IV amoxicillin + cefotaxime

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31
Q

Complications of Bacterial Meningitis

A 
Disseminated Intravascular Coagulation
Vasculitis 
Cerebral Oedema 
Hydrocephalus 
Epilepsy 
Sensorineural hearing loss
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32
Q

Causative Organisms of Bacterial Meningitis in 0-3 months

A

Group B streptococcus
E Coli
Listeria monocytogenes

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33
Q

Causative Organisms of Bacterial Meningitis in 3 months - 6 years

A

Neisseria meningitidis
Streptococcus pneumonia
Haemophilus influenzae

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34
Q

Causative Organisms of Bacterial Meningitis in 6-60 years

A

Neisseria meningitidis

Streptococcus pneumoniae

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35
Q

Causative Organisms of Bacterial Meningitis in > 60 years

A

Streptococcus pneumoniae
Neisseria meningitidis
Listerior monocytogenes

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36
Q

Causative Organisms of Bacterial Meningitis in immunosuppressed

A

Listeria monocytogenes

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37
Q

Group B streptococcus meningitis

A

Most common cause in neonates
Acquired during passage through birth canal
Common if low birth weight and prolonged rupture of membranes

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38
Q

Listeria monocytogenes meningitis

A

Found in pate, raw veg/salad, unpasteurised milk/cheese (foods avoided during pregnancy)
Resistant to cephalosporins

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39
Q

Neisseria meningitidis

A

Upper RT commensal found in nasopharynx and tonsils.

Cause of meningitis in 3 months and older.

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40
Q

Presentation of TB meningitis

A

Fulminant - similar to bacterial meningitis

Insidious - headache, confusion and CN deficits over weeks to months

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41
Q

Fundoscopy in TB meningitis

A

Choroidal tuberculosis

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42
Q

Management of TB meningitis

A

Rifampicin, Isoniazid, Pyrazinamide and Ethambutol for 2 months

Rifampicin and Isoniazid for following 2 months

Steroids if severe e.g. tuberculoma, progression to next stage

Surgical decompression if hydrocephalus occurs

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43
Q

Types of neurosyphilis

A 
Endarteritis obliterans 
Tabes dorsalis
Dementia paralytica 
Gummas 
Acute meningitis
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44
Q

Endarteritis obliterans

A

lymphoplasmacytic meningitis

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45
Q

Tabes dorsalis

A

Inflammation and degeneration of posterior columns of spinal cord

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46
Q

Dementia paralytics

A

encephalitis due to invasion of brain by spirochetes

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47
Q

Gummas

A

Rubbery necrotic and inflammatory mass containing spirocetes. Acts like a space occupying lesion

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48
Q

Presentation of neurosyphilis

A

General meningitis symptoms - headache, confusion, N&V, stiff neck (Endarteritis obliterans/ Lymphoplasmacytic meningitis)

Argyll-Robertson Pupil - Accommodation Reflex Present, Pupillary Reflex Present. Irregular pupils

Forgetfulness & personality change - General paresis of the insane

Loss of proprioception and vibration sense - Tabes dorsalis

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49
Q

Argyll-Robertson Pupil

A

Accommodation Reflex Present, Pupillary Reflex Present. Irregular pupils

Seen in Tabes dorsalis (neurosyphilis) and DM

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50
Q

Management of neurosyphilis

A

IV acqueous benxylpenicillin & oral probenicid

Probenicid causes uric acid secretion. Used to treat gout.

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51
Q

General Features of Lyme Disease

A 
Erythema migrans within 1-2 weeks
Fever
Headache
Myalgia
Fatigue
Arthralgia
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52
Q

Erythema migrans

A

Target lesion on the skin seen in Lyme disease

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53
Q

Borrelia Burgdorferi

A

Tick-borne spirochete causing Lyme disease

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54
Q

Neurological complications of Lyme disease

A

Meningitis
CN palsies (esp. CN VII)
Radiculopathy - Banwarth Syndrome causes pain from spinal column
Peripheral Neuropathy - glove and stocking
Mononeuritis multiplex
Cerebellar ataxia (RARE)
Encephalomyelitis (RARE)

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55
Q

Neuropathy screen

A

HIV, syphilis, HbA1c, TFTs, B12, autoantibodies, CMV, HBV and HCV, sarcoidosis (ACE and CXR)

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56
Q

Management of lyme disease

A

Early Disease: Doxycycline OR Amoxicillin OR Cefuroxime

Neurological disease: Doxycycline OR Ceftriaxone if more serious

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57
Q

Most common fungal infections of CNS

A

Candidiasis > Aspergillus > Cryptococcus

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58
Q

Fungal CSF

A 
Normal or high opening pressure
Low glucose 
High protein 
Mononuclear pleocytosis 
Turbid appearance
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59
Q

Risk Factors for candida infection in the CNS

A 
Catheters
Broad-spectrum 
Antibiotics 
Parenteral nutrition
Immunosuppression
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60
Q

Toxoplasmosis

A

Protozoa. Ingested by other animals. Forms tissue cysts which invade brain, heart and skeletal muscle.
Reproduces in intestinal tract of cats. Usually associated with poorly cooked meat.

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61
Q

Risk factors for toxoplasmosis

A

Immunosuppression
Ingestion of raw or undercooked meat
Exposure to cat faeces

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62
Q

Presentation of toxoplasmosis

A 
Headache
Confusion
Fever
Focal neurological deficit 
Mental status change 
Seizures
Coma
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63
Q

Toxoplasmosis in pregnancy

A

Can cross the placenta and cause necrotising encephalitis and chorioretinitis in foetus.
Leads to severe brain damage, microcephaly, cerebral calcifications and blindness

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64
Q

Diagnosis of Toxoplasmosis

A

Compatible clinical syndrome
Positive T.gondii antibody
Multiple ring enhancing lesions on MRI

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65
Q

Management of toxoplasmosis

A

Sulfadiazine and pyrimethamine

Leucovorin - to prevent pyrimethamine-induced haematological toxicity

Adjuncts:
Dexamethasone if related focal brain lesions or oedema
Anticonvulsants

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66
Q

Psychiatric complications of toxoplasmosis

A

Schizophrenia and suicide

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67
Q

Viral meningitis is most commonly associated with…

A

Enteroviruses

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68
Q

Presentation of viral meningitis

A

RF:
Exposure to insect vectors
Young or old

Headache 
Neck stiffness (rarely kernig’s and Brudzinski’s signs)
N&amp;V
Photophobia 
Fever 
\+/- rash
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69
Q

Management of viral meningitis

A

If patient is very ill, it is reasonable to assume bacterial meningitis and treat accordingly. Wait for CSF results if more stable.

Confirmed viral meningitis = supportive care
Analgesia and antipyretics
Antiemetics if vomiting
IV fluids if dehydrated
Antivirals for: HSV, VZV or CMV (Aciclovir)

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70
Q

Encephalitis

A

Encephalitis is defined as inflammation of brain parenchyma, associated with neurological dysfunction e.g. altered consciousness, seizures, personality change, CN palsy, speech, motor and sensory deficits.

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71
Q

Presentation of encephalitis

A 
Fever
Rash 
Altered mental state 
Focal neurological deficit - CN palsy, aphasia, ataxia, hemiparesis 
Meningismus

Encephalitis can present with altered mental status, motor and sensory deficits, altered behaviour and personality changes. These features are absent in meningitis.

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72
Q

CSF analysis in encephalitis

A 
Pleocytosis (early neutrophils, late lymphocytes)
Elevated erythrocytes 
Elevated protein 
Glucose normal 
PCR is diagnostic (gold standard)
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73
Q

Presentation of HSV encephalitis

A

Affects temporal and inferior frontal lobes.

Causes bizarre behaviour, personality change, anosmia, gustatory hallucination.

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74
Q

Pathology of poliomyelitis

A

Affects grey matter.

Spinal cord - paralysis and subsequent denervation atrophy of muscle

Brainstem - cranial neuropathies, neurogenic pulmonary oedema

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75
Q

Presentation of poliomyelitis

A

90% asymptomatic
Minor illness = GI
Major illness = acute flaccid paralysis of a single affected limb with muscle atrophy, decreased tendon reflexes and tone

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76
Q

Management of poliomyelitis

A

No cure - supportive treatment only

Physiotherapy and mobilisation

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77
Q

Post-poliomyelitis syndrome

A

Fatigue, weakness and wasting of affected muscles. Requires mobilisation and physiotherapy

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78
Q

Presentation of West Nile Virus

A

Fever THEN change in mental status THEN coma

May have severe asymmetric areflexic weakness or complete flaccid paralysis. More frequently elderly patients.

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79
Q

Zika virus

A

Most asymptomatic but 20% have non specific symptoms resembling dengue fever.
Causes microcephaly in babies born to infected mothers. Placenta is small → IUGR

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80
Q

Neurological manifestations of HIV

A

Direct: HIV encephalitis (AIDS-dementia complex)

Indirect: CNS Toxoplasmosis
Cryptococcosis
CMV encephalitis

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81
Q

Presentation of HIV encephalitis

A

Memory loss
Intellectual deterioration
Behavioural changes
Motor deficits

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82
Q

Receptor associated with autoimmune encephalitis

A

Anti NMDA receptor

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83
Q

Presentation of Autoimmune Encephalitis

A

Young females with ovarian, mediastinal and other teratomas.
Males with testicular teratomas

Prominent Psychiatric features (Anxiety, Bizarre behaviour, Hallucinations, Delusions, Disorganised thinking, Memory disturbance)

Speech disorder
Seizures 
Dyskinesias - orofacial, dystonia, rigidity, opisthotonic postures 
Decreased consciousness 
Autonomic instability
Hypoventilation
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84
Q

Management of Autoimmune Encephalitis

A

IV methylprednisolone +/- IV Ig OR Plasma exchange

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85
Q

Creutzfeldt-Jakob Disease

A

Dementia - Behaviour and personality changes

Visual disturbance

Movement problems - Myoclonus, Ataxia

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86
Q

Risk Factors for Creutzfeldt-Jakob Disease

A

Genetic predisposition
Prion-contaminated instruments
Transfusion or blood or blood products
Consumption of UK beef from 1980-1996

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87
Q

Management of Creutzfeldt-Jakob Disease

A

Symptom management

  • Benzodiazepines for anxiety/restlessness and myoclonus
  • SSRIs for depression
  • Antipsychotics for psychosis
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88
Q

Presentation of Tetanus

A 
Lock jaw (trismus)
Back pain
Muscle stiffness (hypertonia)
Dysphagia 
Spasms
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89
Q

Management of potential tetanus exposure

A

Wound debridement

Tetanus vaccine +/- tetanus immunoglobulin

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90
Q

Management of clinical tetanus (Hypertonia)

A

Supportive care
Benzodiazepines for painful muscle spasms
Metronidazole
Tetanus Ig if severe
Magnesium Sulphate (presynaptic neuromuscular blockade)

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91
Q

Presentation of Botulism

A 
Blurred/Double vision
Ptosis 
Dysarthria
Dysphagia
Symmetrical, descending flaccid paralysis
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92
Q

Risk Factors for Botulism

A

Ingestion of contaminated foods (home-canned vegetables)
Infants
Biological terrorism

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93
Q

Management of Botulism

A

Botulism antitoxin

Debridement of any wound infection

Mechanical ventilation if upper airway compromise

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94
Q

Lyssavirus

A

Rabies

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95
Q

Transmission of rabies

A

Animal bites

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96
Q

Presentation of rabies

A 
Encephalitis 
Hypersalivation
Choking sensation when offered a drink - severe laryngeal and diaphragmatic spasm
Perspiration
Priapism - persistent, painful erection
Agitation &amp; hallucination
Weakness
Reduced sensation
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97
Q

Prognosis for rabies

A

Fatal once symptomatic

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98
Q

Management of rabies

A

Aymptomatic: Rabies Ig and wound cleansing

Symptomatic: Palliative care

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99
Q

Cystericosis

A

Most common parasitic disease of CNS (Taenia Solium) - TAPEWORM
Most common cause of epilepsy worldwide

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100
Q

Presentation of cystericosis

A

New onset seizures
Hepatomegaly
Cough and haemoptysis
Worm segments in stool

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101
Q

Risk Factors for Cystericosis

A 
Living on farms 
Poor hygiene 
Eating or handling undercooked meat or fish
Ingestion of contaminated water 
Dog owners 
Children
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102
Q

Management of Cystericosis

A

Antihelminthic - praziquantel or albendazole

If CNS disease - corticosteroid and antiepileptic

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103
Q

Features of subfalcial herniation

A

Drowsiness
Progressive LOC
One-sided weakness
+/- Late visual disturbance

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104
Q

Features of uncal herniation

A

Visual disturbance then LOC

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105
Q

Features of Central Herniation

A

Drowsiness and impaired consciousness then visual disturbance

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106
Q

Features of Rostrocaudal herniation

A

Abrupt LOC
Visual, hearing and taste disturbance
+/- differences in facial expression or movement

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107
Q

Features of Tonsillar Herniation

A

Difficulty breathing then coma

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108
Q

GCS scoring:

Opens eyes when you speak to them

A

E3

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109
Q

GCS Scoring:

Opens eyes on sternal rub

A

E2

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110
Q

GCS Scoring:

Localises pain on sternal rub

A

M5

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111
Q

GCS Scoring:

Withdraws by flexion in response to sternal rub

A

M4

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112
Q

GCS Scoring:

Decorticate posture/Abnormal flexion

(Flexed elbows and wrists, feet turned in)

A

M3

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113
Q

GCS Scoring:

Decerebrate posture/Abnormal extension

(Extended elbows, wrists flexed outwards, toes pointed)

A

M2

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114
Q

GCS Scoring:

Confusion

A

V4

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115
Q

GCS Scoring:

Inappropriate words

A

V3

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116
Q

GCS Scoring:

Incomprehensible sounds

A

V2

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117
Q

Dysfunction associated with Decorticate posture

A

Problems with cervical spinal tract or cerebral hemisphere

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118
Q

Dysfunction associated with Decerebrate posutre

A

Problems with midbrain or pons

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119
Q

Normal response to Caloric Testing in coma

A

When irrigating ear with cold water, eyes should deviate to side of irrigation and there will be a nystagmus

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120
Q

FOUR Score

A

More detailed assessment of the unconscious patient (better than GCS)

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121
Q

Pinpoint pupils are associated with dysfunction of which structure

A

Pons

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122
Q

Dilate, fixed pupil is associated with…

A

CN III palsy

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123
Q

Function and components of Reticular Activating System

A

Inducing and maintaining alertness

Thalamus, Hypothalamus, pituitary gland, Midbrain, Rostral Pons, Cerebral Hemispheres

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124
Q

Indication for immediate CT head

A

GCS < 13 immediately after injury
GCS < 15 2 hours after injury
Suspected open or depression skull fracture
Signs of base of skull fracture (haemotympanum, panda eyes, CSF leak from ear or nose, Battle’s sign)
Post traumatic seizure
Focal neurological deficit
> 1 episode of vomiting

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125
Q

Pathology of Wernicke’s Encephalopathy

A

Exhausted B-vitamin reserves, particularly Thiamine/B1

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126
Q

Presentation of Wernicke’s Encephalopathy

A 
Ataxia 
Ophthalmoplegia 
Encephalopathy 
Hypothermia 
Coma 
Preserved pupillary reflexes 
Ocular movement palsies of absent vestibular-ocular reflexes
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127
Q

Risk Factors for Wernicke’s Encephalopathy

A

Nutritionally deprived patients
Alcoholics
Those with gastric stapling
Patients on haemodialysis not taking B vitamin supplements

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128
Q

Management of Wernicke’s Encephalopathy

A

ABCD approach
IV thiamine 50-100mg
Correction of Mg2+ deficiency
Multivitamin supplementation

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129
Q

General seizures affect one or both sides of the brain?

A

Both sides

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130
Q

Focal/Partial seizures affect one or both sides of the brain

A

One side. May start in a specific area

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131
Q

During what type of seizures might patients have awareness

A

Focal/Partial

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132
Q

During what type of seizures to patients lose consciousness

A

Generalised

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133
Q

Features of Temporal Lobe Focal Seizures

A

Hallucinations
Epigastric rising/Emotional
Automatisms (lip smacking, grabbing)
Déjà vu

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134
Q

Features of Frontal Lobe Seizures

A

Head/Leg movements
Posturing
Postictal weakness

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135
Q

Todd’s Paralysis

A

Affected limb becomes temporarily weak after a Frontal Lobe Focal seizure

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136
Q

Features of Parietal Lobe Seizures

A

Paraesthesiae

Sensory disturbance - tingling, numbness, pain
Motor symptoms - spread to precentral gyrus

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137
Q

Features of Occipital Lobe Seizures

A

Flashes or floaters

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138
Q

Features of Tonic Clonic Seizures

A

Hypertonia - usually fall backwards, may cry out or bit their tongue
Clonus - rhythmic relaxing and contracting of muscles, noisy breathing, wet themself
Breathing and colour return to normal. Feeling tired and confused

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139
Q

Features of Clonic seizures

A

Repeated rhythmic jerking movements

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140
Q

Features of Tonic seizures

A

Sudden hypertonia. Usually fall over backwards if standing. Brief.

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141
Q

Features of Atonic seizures

A

‘Drop attack’. Usually fall forwards and may injure head or front of face.

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142
Q

Features of Myoclonic Seizures

A

‘Muscle jerk’. Brief, can occur in clusters, usually after waking.

Conscious but classified as generalised as they are normally accompanied by other types of seizures.

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143
Q

Features of Absence seizures

A

Children > adults
Looking blank, staring or fluttering of eyelids.
Can carry on walking if they are already walking.

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144
Q

Differentials for Absence seizures

A

Daydreaming
ADHD
Complex focal epilepsy (Frontal or temporal)

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145
Q

Indication for drug treatment in epilepsy

A

2+ attacks in 2 years

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146
Q

First line management of focal seizures

A

Carbamazepine or Lamotrigine

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147
Q

Second line management of focal seizures

A

Levetiracetam, oxcarbazepine, sodium valproate

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148
Q

First line management of Generalised Tonic Clonic Seizures

A

Sodium Valproate

Lamotrigine for females of childbearing age

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149
Q

Second line management of Generalised Tonic Clonic Seizures

A

Carbamazepine, Clobazam, levetiracetam, topiramate

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150
Q

First line management of absence seizures

A

Sodium valproate or ethosuximide

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151
Q

Second line management of absence seizures

A

Lamotrigine

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152
Q

First line management of myoclonic seizures

A

Sodium valproate

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153
Q

Second line management of myoclonic seizures

A

Levetiracetam, topiramate (ADRs)

Avoid carbamazepine and oxcarbazepine as they may worsen seizures

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154
Q

First line management of Tonic/Atonic seizures

A

Sodium valproate or Lamotrigine

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155
Q

MOA of Sodium valproate

A

GABA transaminase inhibitor

i.e. increased inhibitory effect of GABA

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156
Q

ADRs of Sodium Valproate

A 
P450 inhibitor
Teratogenic 
GI: Nausea 
Alopecia - regrowth curly 
Ataxia 
Tremor 
Hepatitis 
Pancreatitis 
Thrombocytopenia 
Hyponatraemia
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157
Q

Effect of Sodium Valproate on drug metabolism

A

P450 inhibitor i.e. inhibits breakdown of other drugs, increasing their effect

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158
Q

Contraindications of Sodium Valproate

A

Females of reproductive age
Pregnant women
Breastfeeding

Hepatic dysfunction

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159
Q

MOA of Lamotrigine

A

Na+ channel inhibitor

Stabilises neuronal membranes and modulates glutamate release

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160
Q

ADRs of Lamotrigine

A

Exacerbation of myoclonic seizures
Aggression or agitation
Drowsiness or fatigue

Stevens-Johnson Syndrome (flu-like + rash w/ blisters)

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161
Q

Lamotrigine should be used with caution if…

A

Myoclonic Seizures

Parkinson’s disease

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162
Q

MOA of Carbamazepine

A

Na+ channel blockade - inhibits synaptic transmission in spinal cord. Effects in trigeminal nuclei cause analgesia.

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163
Q

ADRs of Carbamazepine

A 
P450 inducer (reduces effect of other drugs)
Dizziness
Ataxia 
Headache 
Visual disturbance - DIPLOPIA
Steven-Johnson Syndrome 
SIADH
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164
Q

Effect of carbamazepine on drug metabolism

A

P450 inducer - increases metabolism of drugs therefore reducing their effects

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165
Q

Contraindications for Carbamazepine

A

Acute porphyrias
AV conduction abnormalities
History of bone marrow suppression

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166
Q

MOA of Ethosuximide

A

Ca2+ channel blockade

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167
Q

Indication for Ethosuximide

A

Absence seizures

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168
Q

ADRs of Ethosuximide

A

MANY

Agranulocytosis
Impaired concentration
GI disorders
Stevens-Johnson Syndrome

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169
Q

Contraindications for Ethosuximide

A

Acute Porphyrias

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170
Q

DVLA rules for seizures

A

Patient must inform DVLA and be 1 year seizure free before driving
6 months seizure free if single seizure only

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171
Q

Definition of Status Epilepticus

A

State of continued seizures for more than 5 minutes without regaining consciousness

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172
Q

Risk Factors for Status Epilepticus

A 
Non adherence to medication
Chronic alcoholism 
Refractory epilepsy
Toxic or metabolic causes 
Direct cortical structural damage 
Drug use 
Tramadol lowers seizure threshold
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173
Q

Management of Status Epilepticus

A

ABCDE approach

Add thiamine and glucose if hypoglycaemic

IV Lorazepam 0.1mg/kg (Or IV diazepam or Buccal midazolam if no IV access) - administer 2 doses before 2nd line therapy below.

20mg/kg IV phenytoin if no effect + ECG monitoring

General Anaesthesia: Rapid sequence induction (propofol)

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174
Q

Features of Tension Headache

A

Bilateral, tight band sensation
Associated with stress
Tension and tenderness in neck and scalp muscles.
Mild to moderate

Not aggravated by physical activity

+/- photosensitivity or phonosensitivity

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175
Q

Management of Tension Headache

A

Simple analgesia

Avoid triggers

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176
Q

Features of Cluster Headache

A 
Short attacks around the eye
Rapid onset 
Last 30 mins to 3 hours 
1-2x/day for 1-3 months 
Associated with lacrimation, flushing, conjunctivitis, eyelid swelling, Horner’s syndrome during attack (ipsilateral)
Males, 20s, smokers
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177
Q

Management of Cluster Headache

A

Acute: 100% O2 & Triptan

Prophylaxis: Verapamil

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178
Q

Criteria for migraine diagnosis

A

A - At least 5 attacks. Meeting B, C, D and E.

B - Last 4-72 hours

C - 2 or more of the following: Pulsing, Severe, Unilateral, Aggravated by or causing avoidance of routine daily activities

D - 1 of the following:
Nausea +/- vomiting, Photophobia and phonophobia

E - cannot be attributed to another cause

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179
Q

Management of Migraine

A

Abortive;
Paracetamol or Triptan

Preventative: Propranolol, Pizotifen, Amitriptyline

Pregnancy: Paracetamol is first line, Aspirin/Ibuprofen can be 1st or 2nd line in 1st and 2nd trimester

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180
Q

Features of medication overuse headache

A

Present for 15 days or more per month.
Developed or worsened whilst taking regular medication.
Patients using opioids and triptans are most at risk
May be psychiatric comorbidity

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181
Q

Features of Trigeminal Neuralgia

A

Stabbing pain in unilateral trigeminal nerve region
Face screws up with pain
Triggered by washing, shaving, talking or underlying cause e.g. tumour, MS, aneurysm

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182
Q

Risk Factors for Trigeminal Neuralgia

A

MS
HTN
Age
Female

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183
Q

Management of Trigeminal Neuralgia

A

MRI to find cause

Antiepileptics e.g. 1st line carbamazepine. 2nd line Baclofen

Ablative surgery/Neurostimulation

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184
Q

Most common cause of SAH

A

Trauma

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185
Q

Most common pathology of SAH

A

Berry aneurysms

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186
Q

Risk Factors for SAH

A 
HTN
Smoking
FHx
AD Polycystic Kidney Disease
Coarctation of aorta
Ehlos Danlos Syndrome
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187
Q

Features of SAH

A 
‘Thunderclap’ headache 
Occipital in nature
N&amp;V
Meningism (photophobia and neck stiffness)
Coma
Seizures 
Sudden death
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188
Q

Diagnosis of SAH

A

CT - acute, hyperdense/bright blood in basal cisterns, sulci +/- ventricular system
LP - 12 hours after onset of symptoms, xanthochromia

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189
Q

Management of SAH

A

Coiling of intracranial aneurysm by interventional radiologist OR craniotomy & clipping by neurosurgeon (rare)

Strict bed rest + Well controlled blood pressure + Avoid straining to prevent rebleed

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190
Q

Features of Subdural Haematoma

A

Elderly
Those on anticoagulants

Usually following head injury 
There may be a long interval between injury and presentation (days/weeks/month)
Headache 
Drowsiness &amp; Confusion 
Hemiparesis and sensory loss 
Epilepsy (occasionally)
Stupor, coma and coning (later)
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191
Q

Features of Extradural Haemorrhage

A

Usually young
(Dura is less adherent to the skull in the young)

Following a linear skull vault fracture
Brief duration of unconsciousness followed by improvement (lucid interval)
Stupor
Ipsilateral dilated pupil
Contralateral hemiparesis
Uncal Herniation → bilateral fixed pupils, tetraplegia and respiratory arrest

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192
Q

Management of Subdural Haematoma

A

Less immediate treatment than extradural.

Imaging and monitoring - bleeds can usually drain spontaneously

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193
Q

Management of Extradural Haematoma

A

Urgent neurosurgery for drainage

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194
Q

Complications of SAH

A

Vasospasm

Obstructive Hydrocephalus

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195
Q

Management of Vasospasm in SAH

A

Prophylaxis: Nimodipine (CCB targeting brain vasculature) - 21-day course

Treatment: hypervolaemia, induced-hypertension and haemodilution

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196
Q

Management of Obstructive Hydrocephalus in SAH

A

External ventricular drain (CSF diverted into a bag at the bedside)

197
Q

Features of Amyotrophic Lateral Sclerosis

A 
Muscle weakness and wasting 
Fasciculations 
Cramps 
Brisk reflexes 
Extensor plantar responses 
Spasticity

Single limb initially, progresses to other limbs and trunk

Progression takes place over months

198
Q

Presentation of Progressive Bulbar Palsy

A

Dysarthria THEN Dysphagia
Nasal regurgitation of fluids
Choking
Fasciculating tongue with slow, stiff tongue movements
Emotional incontinence i.e. pathological laughter and crying

199
Q

Diagnosis of MND

A

Upper and lower motor neuron signs
EMG shows active and chronic partial denervation
Relentless progression of signs and symptoms

200
Q

Complications of MND

A

Respiratory failure - inadequate ventilation, hypoxaemia, ineffective cough, risk of aspiration

Feeding difficulty

VTE

201
Q

Indications for ventilatory support in MND

A

Acute - cardiorespiratory arrest, respiratory distress, blood gas abnormality, severe bulbar dysfunction, impaired consciousness

Chronic - VC < 60% predicted, FVC < 50% predicted

202
Q

Problems with NIV

A

Mask causes skin breakdown - cannot be used long term

Unsuccessful if severe bulbar dysfunction, upper airway obstruction or retention of respiratory secretions

203
Q

Indications for Tracheostomy in MND

A

Difficulty clearing secretions

Progressive chronic respiratory failure requiring intermittent long-term mechanical ventilation but NIV contraindicated or insufficient e.g. severe bulbar dysfunction

Patients who fail to wean off invasive mechanical ventilation

204
Q

Management of VTE risk in MND

A

Educate patient and family on signs and symptoms

Antiembolism stockings + devices e.g. intermittent pneumatic compression

Pharmacological - Fondaparinux, LMWH or Heparin

205
Q

Stages of a Swallowing Assessment

A

Inspect patient, especially lips and tongue
Examine CN V, VII and IX including gag reflex

Assess swallow using a cracker, thickened fluid and water. Feel their neck when swallowing. Ask them to say ‘ah’ when finished and listen for rattling.

206
Q

Pathology of Parkinson’s Disease

A

Dopaminergic Neurons in Substantia Nigra are replaced with Lewy Bodies.

207
Q

Key Features of Parkinsonism

A

Akinesia
Bradykinesia
Cogwheel Rigidity (occurs throughout the range of movement)
Resting tremor
Shuffling gate + freezing e.g. when walking through a doorway

208
Q

Earliest sign of Parkinson’s

A

Anosmia

209
Q

Complications in Parkinson’s

A

Increased risk of falls
Increased risk of fractures (osteoporosis)
Dementia
Psychiatric illness

210
Q

Sleep problems seen in Parkinson’s

A

Restless legs
REM sleep behaviour - hitting out
Excessive daytime somnolence
Sudden onset sleep

211
Q

First line treatment of Parkinson’s symptoms which are affecting daily life

A

Co-careldopa (levodopa with carbidopa) or Co-beneldopa (Levodopa with Benserazide)

i.e. L-dopa containing drugs and dopa-decarboxylase inhibitor to prevent peripheral conversion to dopamine

212
Q

ADRs of Levodopa

A

ADRs: Dyskinesia, Painful dystonia

Psychosis, visual hallucinations and N&V → non motor ADRs treated with Domperidone

213
Q

Symptoms of levodopa withdrawal

A

Acute Akinesia in response to sudden withdrawal

Often misdiagnosed as Neuroleptic Malignant Syndrome

214
Q

First line treatment of Parkinson’s disease without affect on daily life

A

Dopamine agonists e.g. Ropinirole, Pramipexole

MAO-B Inhibitors e.g. Rasagiline, Selegiline

215
Q

ADRs of Dopamine agonists e.g. Ropinirole

A

Drowsiness, Nausea, Hallucinations, Compulsive behaviour (gambling, hypersexuality - both are reversible).

216
Q

ADRs of MAO-B inhibitors e.g. Rasagiline

A

Postural hypotension, AF

217
Q

Management of sleep disorders in Parkinson’s

A

Modafinil for daytime somnolence

Clonazepam or melatonin for REM sleep disorder

218
Q

Management of orthostatic hypotension in Parkinson’s

A

Midodrine (alpha agonist - vasopressor)

Fludrocortisone (mineralocorticoid effects)

219
Q

Management of hallucinations and delusions in Parkinson’s

A

Do not treat if well tolerated
Quetiapine (2nd generation antipsychotic)
Clozapine (5-HT antagonist)

Avoid olanzapine and other dopaminergic drugs.

220
Q

Management of drooling in Parkinson’s

A

Glycopyrronium bromide
Specialist referral for Botulinum toxin A
Anticholinergics if cognitive impairment is minimal

221
Q

Management of dementia in Parkinson’s

A 
Acetylcholinesterase inhibitors (e.g. donepezil, rivastigmine)
Memantine
222
Q

Features of Progressive Supranuclear Palsy

A

Similar to Parkinson’s Abnormal eye movements (unable to look upwards)

223
Q

Features of Multisystem Atrophy

A 
Similar to Parkinson's  
Rigidity > tremor 
Autonomic dysfunction e.g. incontinence, postural hypotension 
Cerebellar signs
No dementia
224
Q

Features of Corticobasal Degeneration

A 
Similar to Parkinson's 
Akinetic rigidity of one limb
Sensory loss (astereognosis)
Apraxia 
Early cognitive impairment
225
Q

Chorea

A

Brief, abrupt, irregular, unpredictable, stereotypes movements.

i.e. very fidgety

226
Q

Pathology of Huntington’s disease

A

AD
Trinucleotide repeat disorder (CAG repeat)

Causes degeneration of cholinergic and BAGAergic neurons in striatum of basal ganglia.

227
Q

Features of Huntington’s disease

A

> 35 yrs
Chorea
Personality change - irritable, depressed
Intellectual impairment
Dystonia
Saccadic eye movement
Low BMI - difficulty swallowing and high calorific demand

Often have a family history

228
Q

Management of Huntington’s disease

A

Counselling for patient and family

Symptomatic, MDT approach

229
Q

Presentation of Benign Hereditary Chorea

A

Mild chorea and hypotonia from infancy.

Frequently improves with age and does not progress

230
Q

Definition of a ‘tic’

A

Brief, sudden, repetitive movements or sounds (stereotyped). Preceded by an inner urge or local premonitory sensation which is relieved by performing the tic. Increased with stress, anxiety and excitement, decreased by distraction.

They CAN be suppressed temporarily UNLIKE focal seizures (DDx).

231
Q

Criteria for Tourette’s Syndrome

A

Multiple motor tics & at least 1 phonic tic (Echolalia - repeating something someone else has said, Coprolalia - swearing)

Starts under the age of 18 yrs

232
Q

Risk Factors for Tic Disorders

A 
< 18 years
Male
Family history of tics or OCD
ADHD
Depression 
Behavioural disorder e.g. ADHD or OCD
233
Q

Secondary causes of Tic disorders

A 
Infections 
Substance abuse usually stimulants 
Medicine e.g. Lamotrigine 
Toxins e.g. carbon monoxide 
Head trauma 
Stroke 
Metabolic and endocrine (chorea gravidarum, thyrotoxicosis)
Neurodegenerative (HD, Wilson’s)
234
Q

Conservative management of Tic Disorders

A

Comprehensive behavioural intervention for tics
Habit-reversal training
CBT

235
Q

Pharmacological management of Tic Disorders

A

First line: Alpha-2-adrenergic agonists e.g. Clonidine
Second line: Topiramate (vg Na+ and Ca2+ channel blockade, excitatory glutamate inhibitor)
Third line: atypical neuroleptics e.g. Aripiprazole or risperidone (for severe disease)

236
Q

Presentation of Dystonia

A

Sustained, involuntary contractions of agonist and antagonist muscles - loss of coordination of muscle relaxation with contraction. Often leads to repetitive twisting movements and abnormal postures of trunk, neck, face or extremities.

Dystonia appears or gets worse with action

Children - leg movement
Adults - blepharospasm (tight eyelid closure), Cervical torticollis (neck turning)

237
Q

An example of physiological dystonia

A

Writer’s cramp

238
Q

Management of generalised dystonias

A

First line: Levodopa PLUS
Physiotherapy
Antispasmodic e.g. baclofen (GABA-B stimulator), clonazepam
Treatment of underlying disease

Second line: Trihexyphenidyl (centrally-acting muscarinic antagonist) PLUS above

Third line: Deep Brain Stimulation

239
Q

Management of focal dystonia

A

Botulinum toxin is first line +/- TENS

240
Q

Definition of tremor

A

Involuntary rhythmic oscillation of 1+ body parts. Mediated by alternating contractions of reciprocally acting muscles.

241
Q

Deep brain stimulation:

  • Indication
  • Site of action
  • Criteria
A

Used for PD, tremor, dystonia.

Stimulates globus pallidus and thalamus

Not eligible if > 70, cognitive decline or falls.

242
Q

Multiple Sclerosis tends to affect:

A

Periventricular white matter
Optic nerves
Spinal Cord

243
Q

L’hermitte’s phenomenon

A

Neck flexion causes paraesthesiae down the spine.
Caused by a plaque in the spinal cord.

Commonly associated with MS. Differentials include spinal cord compression, B12 deficiency, idiopathic cause.

244
Q

Uhthoff’s phenomenon

A

Worsening of MS symptoms when temperature is raised e.g. during exercise, in the batj

245
Q

Internuclear ophthalmoplegia

A

Classical symptom of MS.

E.g. If the left eye is affected, when looking to the right, left eye adducts minimally and right eye abducts with nystagmus

246
Q

Signs and symptoms of Transverse myelitis

A

Sensory loss - begins distally and ascends, with a level
Weakness e.g. foot dragging or slapping
Urinary symptoms e.g. incontinence, retention, urgency
Bowel symptoms, usually constipation
UMN signs e.g. spasticity, hyperreflexia

247
Q

Signs and symptoms of Optic Neuritis

A

Painful eye movements (dull ache)
Relative Afferent Pupillary Defect (RAPD)
Impaired colour vision - low saturation of red
Visual fields - central scotoma
Reduced visual acuity
Fundoscopy: Optic atrophy, swollen, hyperaemic disc

248
Q

Presentation of MS

A

Transverse myelitis
Optic neuritis
Wide-based gate or limb ataxia if brainstem/cerebellum affected
Cognitive dysfunction if cerebral hemispheres affected

249
Q

Definition of a relapse in MS

A

New neurological symptoms or exacerbation of old symptoms lasting > 24 hours, in the absence of fever or infection. Remission needs to last for at least 30 days between relapses.

Remyelination, reduction of oedema and insertion of Na+ channels into demyelinated nerve membrane are responsible for periods of remission.

250
Q

Most common form of MS

A

Relapsing-remitting (85%)

251
Q

Immune cells responsible for MS

A

T helper cells and macrophages

252
Q

Criteria for MS diagnosis

A

McDonald Criteria

Dissemination in time and space demonstrated by MRI or clinical symptoms

253
Q

Imaging essential for diagnosis of MS

A

MRI brain - hyperintensity in periventricular white matter. Gadolinium used to distinguish active from inactive plaques.

MRI spine

254
Q

CSF evaluation in MS

A

Oligoclonal bands (IgG)

Moderately elevated protein
Mild mononuclear pleocytosis

255
Q

Management of Acute Relapse in MS

A

Methylprednisolone (IV 1g OD for 3 days or PO 500 mg OD for 5 days, give in the morning to reduce insomnia) +/- Plasma exchange
Steroids will only accelerate recovery, not improve outcomes.

Patients can be offered nursing/home support during these episodes.

256
Q

Disease-modifying treatment of MS

A 
Interferon beta 1a/b (SC or IM) - only drug which is licensed in 2o progressive disease
Peginterferon beta 1a
Glatiramer acetate (SC)
Teriflunomide
Dimethyl fumarate
257
Q

Indications for disease modifying treatment in MS

A

2 relapses in the last 2 years
1 disabling relapse in the last year
No substantial progression
Ability to walk

258
Q

Efficacy of Disease Modifying Drugs in MS

A

Reduce relapse rate by ⅓ for 2 years of treatment AND reduce relapse severity.

259
Q

Lifestyle modifications recommended in MS

A

Regular exercise including resistance training to combat fatigue
Good sleep hygiene
Mind-body therapy e.g. yoga

260
Q

Hypersensitivity reaction seen in Myasthenia Gravis

A

Type II

261
Q

Immune cells associated with Myasthenia Gravis

A

B cells and T cells

262
Q

Receptors affected in Myasthenia Gravis

A

Nicotinic ACh receptors

263
Q

Presentation of Myasthenia Gravis

A

Fluctuating muscle weakness, affecting muscle groups in the following order: Extraocular, bulbar, face, neck, limb girdle, trunk.
Muscle fatiguability

Ptosis
Diplopia
Myasthenic snarl on smiling

264
Q

How do male and female patients with Myasthenia Gravis differ?

A

Females are 20-30 yrs with thymic dysplasia.

Males are 60-70 years with thymic atrophy or tumour.

265
Q

EMG findings in Myasthenia Gravis

A

Decremental response to repetitive nerve stimulation

266
Q

Antibodies seen in Myasthenia Gravis

A

Anti-AChR (90%)

Anti-MUSK (Muscle-specific tyrosine kinase)

267
Q

Management of Myasthenia Gravis

A

Symptom control - Neostigmine/Pyridostigmine (Acetylcholinesterase inhibitors)

Immunosuppression: Prednisolone or Azathioprine

Osteoporosis prophylaxis if steroid management.

Surgical: Thymectomy (if poor response to drug treatment)

268
Q

ADRs of Neostigmine/Pyridostigmine

A 
Increased salivation 
Lacrimation 
Sweats 
Vomiting 
Miosis (constriction of pupil of one eye)
269
Q

Myasthenic Crisis

A

Life threatening weakness of respiratory muscles during relapse

270
Q

Management of Myasthenic Crisis

A

Ventilatory support
Plasmapheresis - removes AChR antibodies from circulation OR IV Ig
Identify and treat trigger

271
Q

Pathology of Lambert Eaton Myasthenic Syndrome

A

Anti-voltage-gated Ca2+ channels at neuromuscular junction

Usually associated with small cell lung cancer

272
Q

Risk Factors for Lambert Eaton Myasthenic Syndrome

A

Underlying malignancy (esp. SC lung CA)
Coexisting AI disease
Cigarette smoking
FH of AI disease

273
Q

Features of Lambert Eaton Myasthenic Syndrome

A

Proximal leg weakness and waddling gait - improves with movement
Dry mouth
Areflexia
Impotence

274
Q

EMG findings in Lambert Eaton Myasthenic Syndrome

A

Positive decrement on repetitive nerve stimulation

275
Q

Management of Lambert Eaton Myasthenic Syndrome

A

Treat underlying cause - usually lung CA
Pyridostigmine (AChesterase inhibitor)
Steroids/Azathioprine

276
Q

Features of Myopathy

A

Proximal Weakness
Elevated CK
Myopathic EMG (small motor units)
Irregular, necrotic muscle fibres on biopsy

277
Q

How does denervation atrophy differ from myopathy?

A

Distal weakness
Normal CK
Fibrillations +/- fasciculations on EMG
Normal muscle biopsy

278
Q

Examples of Myopathy

A

Duchenne Muscular Dystrophy
Myotonic Dystrophy
Polymyositis/Dermatomyositis
Inclusion body myositis

279
Q

Myotonic dystrophy affects which age group?

A

Adolescents and young adults

280
Q

Duchenne muscular dystrophy affects which age group?

A

Children

281
Q

Prevalence of Duchenne Muscular dystrophy

A

1 in 4000

282
Q

Inheritance pattern of Myotonic Dystrophy

A

Autosomal dominant

283
Q

Inheritance pattern of Duchenne Muscular Dystrophy

A

X-linked recessive

284
Q

Typical Features of Myotonic Dystrophy

A

‘Slapped’ face - atrophy of face muscles, ptosis, frontal baldness
Myotonia - cannot let go of handshake
Percussion myotonia - muscles become activated by tapping then cannot relax

285
Q

Extramuscular features of Myotonic Dystrophy

A 
Cataracts
Cardiac arrhythmia 
Testicular atrophy 
Gynaecomastia 
Diabetes
286
Q

Children with Duchenne Muscular Dystrophy are normally confined to a wheelchair by the age of:

A

10-12 years

287
Q

Signs and symptoms of Duchenne Muscular Dystrophy

A

Calf pseudohypertrophy
Toe-walking
Gower’s manoeuvre - unable to use proximal muscles to get up off the floor

May have cognitive and behavioural impairment (dystrophin is found in cortical neurons)

288
Q

Complications of Duchenne Muscular Dystrophy

A 
Respiratory insufficiency - causes death by 2nd decade 
Dilated cardiomyopathy (also seen in female carriers)
289
Q

Becker Vs Duchenne Muscular Dystrophy

A

Becker is less severe. Diminished quantity/quality of dystrophin.

290
Q

Management of Myotonic Dystrophy

A

Symptomatic e.g. fitted collar for head-drop, eyelid crutches for ptosis, modafinil for daytime sleepiness

Genetic counselling
Monitoring of extramuscular features
Swallowing assessment

291
Q

Management of Duchenne Muscular Dystrophy

A

Corticosteroids
Physiotherapy + exercise + psychological support
Surgery for contractures
Cardioprotective drugs
Positive pressure ventilation if contractures of lungs & chest wall
Surgery for scoliosis

292
Q

Presentation of Polymyositis

A

Adults with proximal weakness

293
Q

Lymphocytes associated with Polymyositis

A

CD-8

294
Q

Presentation of Dermatomyositis

A

All ages
Proximal weakness + Rash

Purple discolouration of upper eyelids
Oedema around eyes and mouth
Facial erythema
Red scaly papules over extensors

295
Q

Autoantibody associated with Dermatomyositis

A

Anti-Jo-1 autoantibodies

296
Q

Lymphocytes associated with Dermatomyositis

A

CD-4

297
Q

Muscle biopsy findings in Polymyositis

A

Myonecrosis of myomysium

298
Q

Muscle biopsy findings in Dermatomyositis

A

Atrophy of perimysium

299
Q

Features of Inclusion Body Myositis

A

Men, > 50 yrs
Distal muscle weakness - wasting of forearms causing watch to be loose
Elevated CK

300
Q

Causes of Rhabdomyolysis

A 
Trauma
Excessive exertion inc. seizures 
Muscle ischaemia e.g. compartment syndrome 
Infection
Hyperthermia 
Toxins 
Drugs e.g. Statins
301
Q

Presentation of Rhabdomyolysis

A 
Weakness
Myalgia
Muscle swelling
Elevated CK
Red-brown urine (myoglobinuria)
AKI
302
Q

Management of Rhabdomyolysis

A

Fluids

Haemodialysis if anuric or unresponsive to hydration

303
Q

Signs and symptoms of Steroid Myopathy

A

Proximal muscle weakness
Lower extremities then upper
Cushingoid features

304
Q

Non pharmacological treatment of neuropathic pain

A

Hot/Cold pads
Relaxation and Breathing exercises
Staying active
Treatment of mood

305
Q

First line drug management of neuropathic pain

A

Amitriptyline, Duloxetine, Gabapentin, Pregabalin.

If any of these treatments are ineffective, one of the other 3 should be offered.

306
Q

First line drug management of neuropathic pain associated with diabetic neuropathy

A

Duloxetine

307
Q

ADRs of amitriptyline

A

Anticholinergic syndrome - drowsiness, dry mouth, constipation, blurred vision
QT prolongation

308
Q

Contraindications for Amitriptyline

A

Arrhythmias
Mania
Heart block
post-MI recovery

309
Q

Duloxetine should be used with caution in patients with…

A

History of seizures
Raised intraocular pressure
Susceptibility to angle-closure glaucoma

310
Q

Duloxetine MOA

A

SNRI

311
Q

Duloxetine: ADRs

A 
Constipation 
Drowsiness
Dry mouth
Headache 
Weight change
312
Q

Gabapentin: MOA

A

Vg Ca2+ channel blocker. Enhances GABA responses and reduces release of neurotransmitters

313
Q

Gabapentin: ADRs

A 
Anticholinergic syndrome 
Arthralgia 
GI upset 
Increased infection risk
Gynaecomastia 
Hyponatraemia
314
Q

Pregabalin: MOA

A

Vg Ca2+ channel blocker. Inhibiting release of excitatory neurotransmitters

315
Q

Pregabalin: ADRs

A 
Anticholinergic syndrome 
Increased infection risk 
GI upset 
Prolonged QT
Gynaecomastia
316
Q

First line management of trigeminal neuralgia

A

Carbamazepine

317
Q

Autoantibodies associated with Neuromyelitis Optica

A

Anti-Aquaporin-4 (AQP4)

318
Q

How does NMO differ from MS?

A

Long segments of spinal cord demyelination

Optic neuritis is more severe with worse recovery

319
Q

Presentation of NMO

A

Transverse Myelitis +/- Optic neuritis

Attacks occur over days, with varying degrees of recovery over weeks to months

320
Q

CSF findings in NMO

A

Elevated protein
No oligoclonal bands
Neutrophilic pleocytosis during acute attacks

321
Q

Diagnosis of NMO

A

CSF - no oligoclonal bands

MRI spine - longitudinally extensive spinal cord lesion.

322
Q

Management of NMO

A

IV Methylprednisolone.

Plasma exchange if unresponsive to steroids.

Long term immunosuppression (steroid sparing)

323
Q

Pathology of Central Pontine Myelinolysis

A

Degeneration of midline patch of pons through loss of myelin.

Triggered by osmotic stress e.g. rapid correction of hyponatraemia

324
Q

Presentation of Central Pontine Myelinolysis

A

Usually asymptomatic

UMN signs: Babinski, hyperreflexia, spastic paralysis (can be of bulbar muscles causing dysarthria and dysphagia)

Behavioural disturbance

Locked-in syndrome or Coma

325
Q

Management of Central Pontine Myelinolysis

A

Relower sodium

ET intubation and ventilation

326
Q

Prevention of Central pontine myelinolysis

A

Na+ should be raised by no more than 6-8 in any 24 hour period

327
Q

Pathology of communicating hydrocephalus

A

Overproduction or reduced absorption of CSF

328
Q

Differentials for communicating hydrocephalus

A

Choroid plexus papilloma (rare)
Subarachnoid haemorrhage - arachnoid granulations cannot absorb CSF normally.
Meningitis

329
Q

Treatment of Hydrocephalus

A

Ventriculoperitoneal shunt

Dexamethasone to reduce inflammation

Decompressive craniectomy if refractory to other management

330
Q

Pathology of non communicating hydrocephalus

A

Obstruction to flow of CSF

May be due to aqueduct stenosis (gradual), tumour, abscess, cysts.

331
Q

Presentation of communicating hydrocephalus

A 
Signs of raised ICP:
Headaches 
Worse with stooping or straining 
N&amp;V
Papilloedema
332
Q

Presentation of non communicating hydrocephalus

A 
Signs of raised ICP:
Headaches 
Worse with stooping or straining 
N&amp;V
Papilloedema

If acute - may cause rapid LOC and death
If incomplete or gradual - may be asymptomatic

333
Q

CT head findings in hydrocephalus

A

Ventriculomegaly

Enlarged temporal horns of lateral ventricles if acute

334
Q

Management of non communicating hydrocephalus

A

Shunting if long term, Extraventricular drain if short term (E.g. SAH)

Treat underlying cause

Dexamethasone to reduce inflammation

Decompressive craniectomy if refractory to other management

335
Q

Pathology of Normal Pressure Hydrocephalus

A

Gradual increase in pulse pressure in major arteries with age, due to atheroma and calcification.

Brain becomes ischaemic due to high CSF outflow resistance impeding cerebral perfusion.

336
Q

Presentation of Normal pressure hydrocephalus

A

Adam’s triad

  1. Gait disturbance (unresponsive to LDOPA)
  2. Dementia
  3. Urinary incontinence
337
Q

Risk Factors for Normal Pressure Hydrocephalus

A

Age > 65 yrs
Vascular disease
DM

338
Q

Management of Normal Pressure Hydrocephalus

A

Control cardiovascular risk factors
Repeated large volume CSF taps

VP shunt or 3rd ventriculostomy if suitable for surgery.

339
Q

Nerve conduction studies:

Demyelination vs Axonal Neuropathy

A

Demyelination - slowing of conduction

Axonal - Low action potential amplitudes

340
Q

Pathology of Peripheral Neuropathy

A

May be due to axonal degeneration, demyelination or vascular damage

341
Q

Peripheral neuropathy affecting large sensory fibres causes…

A

Pins and needles

342
Q

Peripheral neuropathy affecting small sensory fibres causes…

A

Pain

343
Q

Presentation of Common Peroneal Nerve Injury

A

Foot drop
Weak dorsiflexion
Weak toe extension
Weak foot eversion

344
Q

The common peroneal nerve is vulnerable as it runs along the…

A

Fibular head

345
Q

Meralgia Paraesthetica

A

Burning/Electric shock/numbness in anterolateral thigh region.
Caused by entrapment or compression of lateral cutaneous nerve of thigh

346
Q

Carpal tunnel syndromes is caused by compression of the…

A

Median nerve

347
Q

Examples of mononeuropathies

A

Meralgia Paraesthetica
Carpal tunnel syndrome
Foot drop due to common peroneal nerve injury

348
Q

Symptoms of Carpal Tunnel Syndrome

A

Aching pain in hand and arm, may be worse at night

Tingling/numbness in thumb, index and middle finger - may be relieved by dangling off the bed

349
Q

Signs of Carpal Tunnel Syndrome

A

Sensory loss in median nerve distribution
Wasting of thenar eminence
Weakness of abductor pollicis brevis

350
Q

Management of Carpal Tunnel Syndrome

A

Splinting
Vit B6 supplementation (controversial)
Local steroid injection
Decompressive surgery

351
Q

Presentation of ulnar nerve compression at the level of the elbow

A

Flexion of wrist can only occur with abduction
Loss of abduction and adduction of fingers (interossei paralysed)
Froment’s Sign - unable to hold a piece of paper between thumb and index finger (adductor pollicis paralysis)

Loss of sensation in entire ulnar nerve distribution (medial 1.5 fingers, anterior and posterior)

352
Q

Presentation of ulnar nerve compression at the level of the wrist

A

Paralysis of intrinsic muscles of hand - loss of finger abduction and adduction
Froment’s Sign - unable to hold a piece of paper between thumb and index finger (adductor pollicis paralysis)

Sensory loss over palmar side of medial 1.5 fingers

353
Q

Presentation of radial nerve injury due to dislocated shoulder or fracture of proximal humerus

A

Wrist drop

Loss of sensation over full radial nerve distribution

354
Q

Presentation of radial nerve injury due to humeral shaft fracture

A

Weak elbow extension
Wrist drop
Loss of sensation on dorsal surface of lateral 3 digits and associated palm

355
Q

Presentation of injury to superficial branch of radial nerve in the forearm due to a laceration

A

No motor deficit

Loss of sensation in lateral 3 digits and associated palm

356
Q

Presentation of injury to deep branch of radial nerve in the forearm due to a radial head fracture/dislocation

A

Weak wrist extension
No wrist drop - extensor carpi radialis longus unaffected
No sensory deficit

357
Q

Differentials for Peripheral Polyneuropathy

A

Diabetes - glove and stocking, slowly progressive, painful
Amyloid
Nutritional (B12)
Guillain Barre - rapidly progressive - days to weeks, follows respiratory or GI infection (esp. campylobacter)
Toxic - amiodarone, lead
Hereditary - Charcot-marie tooth, Friedreich’s ataxia
Endocrine
Recurring/Renal
Alcohol
Pb (lead)/Porphyria
Infection - leprosy, HIV, Lyme’s
Systemic - sarcoid, SLE, hypothyroid, syphilis
Tumours - paraneoplastic

358
Q

Most common hereditary Peripheral neuropathy

A

Charcot-Marie Tooth

359
Q

Presentation of Charcot-Marie Tooth

A 
Pes cavus (High arched feet)
Altered gait with loss of heel-toe pattern 
Distal muscle weakness and atrophy 
Hyporeflexia 
Frequently sprained ankles
360
Q

Management of Charcot-Marie Tooth

A

Symptomatic - physiotherapy and orthotics. Orthopaedic surgery if severe.

361
Q

Most common form of Guillain-Barré

A

Acute inflammatory demyelinating neuropathy

362
Q

Typical presentation of Guillain-Barré

A

Paraesthesias in toes and fingers, preceding weakness
Rapidly progressive flaccid weakness (upper limb then lower)
Areflexia
Slurred speech
Back and leg pain

Weakness may affect respiratory muscles, requiring ventilation

363
Q

Miller Fisher Syndrome

A

Guillain-Barré syndrome affecting cranial nerves

Causes ophthalmoplegia, ataxia and areflexia

364
Q

Management of Guillain-Barré Syndrome

A

Supportive treatment
Plasma exchange
IV Ig

365
Q

Erb’s palsy is usually caused by…

A

Falling onto shoulder or traction on neck and shoulder at birth

366
Q

Erb’s palsy is due to a lesion of..

A

Upper brachial plexus (C5/6)

367
Q

Erb’s palsy: Presentation

A

‘Waiter’s tip’
arm internally rotated, extended and slightly adducted
Loss of shoulder abduction and elbow flexion.
Sensory loss in C5/6

368
Q

Klumpke’s palsy is usually caused by…

A

Forceful abduction of arm at birth or following trauma

369
Q

Klumpke’s palsy is due to a lesion of..

A

Lower brachial plexus (C8/T1)

370
Q

Klumpke’s palsy: Presentation

A

‘Claw hand’
Loss of function of intrinsic muscles of hand, long flexors & extensors of fingers
Loss of sensation in C8/T1
+/- Horner’s syndrome

371
Q

Pathology of Radiculopathy

A

Conduction block of spinal nerve and its roots due to nerve compression.

May be due to disc prolapse, neurodegenerative disease of spine, fracture, neoplasm, infection.

372
Q

Signs and Symptoms of Radiculopathy

A

Radicular pain - sharp, stabbing, electric shock radiating down the limb
Asymmetric weakness, atrophy and fasciculations
Sensory loss

Exact symptoms depend on site of injury

373
Q

Red flags of Radiculopathy

A 
Faecal Incontinence 
Urinary retention 
Saddle anaesthesia 
Immunosuppression
IVDU
Chronic steroid use 
Osteoporosis 
New onset in over 50 yrs 
History of malignancy
374
Q

Gold standard imaging for radiculopathy

A

MRI spine > CT spine > X-ray spine

375
Q

Features of radiculopathy of L2-4

A

Back pain radiating to anterior leg and knee

Weak hip flexion, knee extension and leg adduction

376
Q

Features of radiculopathy of L5

A

Back pain radiating down lateral aspect of leg to foot.
Weak foot dorsiflexion, toe extension and foot inversion/eversion
Sensory loss in lateral shin and dorsum of foot.

377
Q

Features of radiculopathy of S1

A

Back pain radiates down posterior leg and into foot.
Weak plantarflexion and toe flexion
Sensory loss on posterior leg and lateral foot.
Loss of ankle reflex

378
Q

Features of Cauda Equina Syndrome

A

Lower back pain
Urinary incontinence or retention
Reduced sensation in perianal area (saddle anaesthesia)
Decreased anal tone

379
Q

Management of radiculopathies

A

Analgesia using WHO pain ladder
Neuropathic pain management (Amitriptyline, Gabapentin, Pregabalin, Duloxetine)

Surgery if pain continues, progressive weakness or spinal cord becomes affected.

380
Q

Features of radiculopathy of C5

A

Neck, shoulder and scapular pain
Lateral arm numbness (axillary nerve area)
Weak shoulder abduction, elbow flexion & forearm supination
Loss of biceps and brachioradialis reflexes

381
Q

Features of radiculopathy of C6

A

Neck, shoulder, scapula, lateral arm, forearm and hand pain
Numbness of lateral forearm, thumb and index finger
Weakness of shoulder abduction & external rotation, elbow flexion & forearm rotation
Loss of biceps and brachioradialis reflexes

382
Q

Features of C7 radiculopathy

A

Neck, shoulder, middle finger and hand pain
Numbness of index and middle finger
Weak elbow and wrist extension, forearm pronation and wrist flexion
Loss of triceps reflex

383
Q

Features of C8 radiculopathy

A

Neck, shoulder, medial forearm, medial hand and finger pain
Numbness in medial forearm, medial 2 digits and hand
Weak wrist extension, finger movements and thumb flexion

384
Q

Features of T1 radiculopathy

A

Pain in neck, medial arm and medial forearm.
Numbness in anterior arm and medial forearm
Weak thumb abduction and flexion
Weak finger ab/adduction

385
Q

Corticospinal tracts decussate in the…

A

Medulla of the brainstem

386
Q

Dorsal column tracts decussate in the…

A

Medulla of the brainstem

387
Q

Spinothalamic tracts decussate in the…

A

Spinal cord

388
Q

Spinal tracts affected by Amyotrophic Lateral Sclerosis

A

Corticospinal tracts - Upper and lower motor neurons

389
Q

Spinal tracts affected by Poliomyelitis

A

Anterior horns of corticospinal tracts - lower motor neurons only

390
Q

Spinal tracts affected by Brown-Sequard Syndrome

A

Lateral corticospinal tract
Dorsal columns
Lateral spinothalamic tract

391
Q

Signs of Brown-Sequard Syndrome

A

Contralateral loss of pain and temperature sensation.
Ipsilateral loss of proprioception and vibration sense.
Ipsilateral spastic paralysis below the level of the lesion

392
Q

Subacute combined degeneration of the spinal cord is caused by

A

Vitamin B12 and E deficiency

393
Q

Tracts affected in subacute combined degeneration of the spinal cord

A

Lateral corticospinal tract
Dorsal columns
Spinocerebellar tracts

394
Q

Features of subacute combined degeneration of the spinal cord

A

Bilateral symptoms. Spastic paresis, loss of proprioception and vibration sense and limb ataxia

395
Q

Tracts affected in Freidrich’s ataxia

A

Lateral corticospinal tract
Dorsal columns
Spinocerebellar tracts

396
Q

Features of Freidrich’s ataxia

A

Bilateral symptoms. Spastic paresis, loss of proprioception and vibration sense and limb ataxia

Plus dysarthria, nystagmus and dysdiadochokinesia

397
Q

Anterior spinal cord syndrome is caused by…

A

Anterior spinal artery occlusion

398
Q

Tracts affected in anterior spinal cord syndrome

A

Lateral corticospinal tract

Lateral spinothalamic tract

399
Q

Features of anterior spinal cord syndrome

A

Bilateral spastic paresis (UMN)
Bilateral loss of pain and temperature sensation
Preserved vibration sense and proprioception.

400
Q

Syrinx

A

Cyst full of CSF causing central cord syndrome

401
Q

Syringomyelia

A

Syrinx (cyst full of CSF) within the spinal cord

402
Q

Syringobulbia

A

Syrinx (cyst full of CSF) within the brainstem

403
Q

Tracts affected in central cord syndrome

A 
Ventral horns (containing motor neurons)
Lateral spinothalamic tracts
404
Q

Features of central cord syndrome

A

Often occurs in cervical spinal cord.
Flaccid paralysis - typically intrinsic hand muscles
Loss of pain and temperature sensation - ‘cape-like’ distribution if in cervical cord

405
Q

Differential diagnosis for posterior cord syndrome

A

Neurosyphilis (Tabes dorsalis)
Combined Subacute Degeneration of Spinal Cord (B12 deficiency)
Trauma
MS

406
Q

Features of posterior cord syndrome

A

Bilateral loss of proprioception and vibration sense

407
Q

Cervical spine injury typically occurs at which vertebral levels?

A

C2 (1/3)

C6-7 (1/2)

408
Q

Definition of spasticity (complication of UMN lesions)

A

Velocity dependent resistance to stretch

409
Q

Treatment of spasticity which is interfering with sleep in UMN lesions

A

First line: Baclofen - GABA derivative

Other options include diazepam, dantrolene, tizanidine and botox

410
Q

Pathology of autonomic dysreflexia in a patient with a spinal cord lesion

A

Excessive sympathetic output in patient with an injury at T6 or above.

Precipitated by noxious stimulus below level of injury - most commonly due to bladder distension. Other causes include UTI, constipation, gallstones, pressure sores and ingrowing toenails.

411
Q

Management of Autonomic Dysreflexia

A

Sit patient upright
Remove tight clothing
Regularly monitor blood pressure
Check for precipitants e.g. catheter obstruction, constipation requiring manual evacuation.

Pharmacological management: Nitrates or nifedipine

412
Q

Presentation of Autonomic Dysreflexia

A 
Bilateral pounding headache 
Elevated BP
Sweating above level of injury
Nasal congestion 
Nausea
Blurred vision

In a patient with spinal cord injury at T6 or above. Precipitated by noxious stimulus below level of injury

413
Q

Prevention of pressure sores in patients with spinal cord injury

A

Position changes every 4-6 hours

414
Q

Most common cause of acute cord compression in patients 16-30 years

A

Trauma

415
Q

Most common cause of acute cord compression in patients 30-50 years

A

Disc disease

416
Q

Most common cause of acute cord compression in patients 40-75 years

A

Malignancy

417
Q

Risk factors for acute cord compression

A 
Trauma
Cancer
Osteoporosis 
High risk occupation/recreation
IVDU
Immunosuppression
418
Q

Presentation of acute cord compression

A

Depends on level of injury.

Back pain
Numbness or paraesthesias
Weakness or paralysis (wasting if chronic)
Bladder or bowel dysfunction 
Hyperreflexia (UMN lesion)
Saddle anaesthesia (Cauda Equina)
419
Q

General management of Acute Cord Compression

A

ABCD approach
VTE prophylaxis
Prevention of gastric stress ulcers - omeprazole
Pressure ulcer prophylaxis

420
Q

Management of traumatic spinal cord compression

A

Spinal immobilisation

Decompression/Stabilisation surgery within 72 hours

421
Q

Management of Cauda Equina Syndrome

A

Emergency decompression within 48 hours of onset of symptoms

422
Q

Management of malignant spinal cord compression

A

Palliative.

Corticosteroids - analgesia, reduce oedema and oncolysis
Laminectomy or vertebrectomy
Radiotherapy

423
Q

Causes of transverse myelitis

A

Most commonly MS and Neuromyelitis optica.

Parainfectious e.g. HSV, HZV, CMV, TB, Syphilis, Lyme

Post vaccination

Autoimmune e.g. SLE, Sjogren’s

Sarcoidosis

Paraneoplastic

424
Q

Broca’s area is involved in…

A

Production of coherent speech

425
Q

Wernicke’s area is involved in…

A

Speech processing and understanding language

426
Q

Signs and Symptoms associated with Posterior Cerebral Artery Stroke

A

Homonymous hemianopia (may be the only symptom)

Prosopagnosia - can’t recognise faces
Alexia - inability to read
Receptive Aphasia (can’t comprehend spoken words)

+/- cerebellar or brainstem signs

427
Q

Signs and Symptoms associated with middle cerebral artery stroke

A

Contralateral face and arm weakness and sensory loss
Mild or no leg weakness
Head and eyes deviate towards lesion.

Broca’s aphasia if left sided.

428
Q

Signs and Symptoms of Anterior Cerebral Artery Stroke

A

Contralateral leg weakness and sensory loss
Mild or no upper extremity involvement.

Broca’s aphasia may occur if left sided.

429
Q

Signs and symptoms of Lacunar stroke

A

Pure motor or pure sensory

+/- Ataxia
+/- Clumsy hand syndrome

Higher cortical function such as language, vision, facial recognition not affected.

430
Q

Most common causes of ischaemic stroke

A

Atherosclerosis or embolism (e.g. from AF)

431
Q

Haemorrhagic strokes are usually caused by…

A 
HTN 
AV malformations 
Vasculitis 
Vascular tumours e.g. haemangioma 
Amyloidosis
432
Q

Signs and symptoms which are essential for diagnosis of stroke

A 
Sudden onset
Maximal symptoms at onset 
Negative symptoms ONLY 
Focal
Unilateral
433
Q

ROSIER

A

Recognition of Stroke in Emergency Room

434
Q

Signs and symptoms which reduce likelihood of stroke

A 
LOC
Acute confusion 
Seizure
Gradual progression 
Multiple recurrent symptoms 
Severe headache 
Isolated memory loss, dizziness, lightheadedness or vertigo
435
Q

Management of Ischaemic stroke

A

Thrombolysis (Alteplase) within 4.5 hours of onset of symptoms.

Dual antiplatelet therapy (Aspirin 300mg and Clopidogrel 75mg) within 24 hours of thrombolysis or within 48 hours of symptom onset if no thrombolysis.

Dual antiplatelet therapy for 3 months then continue Clopidogrel long term.

436
Q

Contraindications for Thrombolysis

A 
Previous intracranial haemorrhage
Seizure at onset of stroke 
Brain tumour 
Stroke or traumatic brain injury in preceding 3 months 
Lumbar puncture in preceding 7 days
GI haemorrhagic in last 3 wks 
Active bleeding
Pregnancy 
Oesophageal varices 
Uncontrolled HTN >200/120mmHg
437
Q

Management of haemorrhagic stroke

A

Omit drugs which exacerbate bleed.

FFP/PCC and vitamin K on warfarin.

Admission to critical care. Usually require intubation and invasive monitoring of blood pressure.

Surgical interventions if unstable.

438
Q

Transient Ischaemic Attack

A

‘Mini-stoke’

Symptoms of stroke which resolve within 24 hours. 15% of ischaemic strokes are preceided by TIA.

439
Q

ABCD2 score

A

Determines risk of stroke after a TIA

Age > 60 - 1 pt
Clinical features unilateral weakness (2 pt) or speech impairment (1 pt)
Duration > 60 minutes (2 pt), < 60 minutes (1 pt)
Diabetes 1 pt

Hospital observation necessary if score > 4

440
Q

Management of TIA

A

Immediate Aspirin 300 mg
Urgent (24 hours) stroke assessment within 24 hours if within 7 days.
Routine stroke assessment (1 week) if more than 7 days ago.

Advise not to drive.

Management of risk factors
Clopidogrel 75mg

Carotid doppler scan

441
Q

Indications for Carotid Artery Endarterectomy

A

Anterior circulation only (only offer doppler if symptoms of anterior circulation)
Must be symptomatic
Stenosis >50% in men and >70% in women

442
Q

Mild Traumatic Brain Injury

A

GCS 13-15

443
Q

Moderate Traumatic Brain Injury

A

GCS 9-12

444
Q

Severe Traumatic Brain Injury

A

3-8

445
Q

Definition of coma

A

GCS 3-8 lasting more than 6 hours

446
Q

Persistent vegetative state

A

State of wakeful unconsciousness at least 1 month after coma.
Patient appears awake and has sleep-wake cycles with no evidence of awareness or responsiveness to any stimuli.
Recovery from this state is rare.

447
Q

Brainstem Death

A

GCS = 3
No spontaneous respiratory effort and absent brainstem reflexes. Recovery considered impossible.
Must be tested for by 2 practitioners, both registered for over 5 years, one a consultant + neither a member of the transplant team.

448
Q

Extradural haematomas usually occur in which region?

Which vessels are responsible for the bleeding?

A

Temporal and parietal areas.

Middle meningeal vessels.

449
Q

Pathology of diffuse axonal injury

A

Stretching of axons due to movement of the brain around a fixed brainstem. Results in axonal swelling due to influx of calcium.

450
Q

Which structures are damaged in diffuse axonal injury?

A

Midline structures e.g. corpus callosum and brainstem

Junctions between white and grey matter

451
Q

Presentation of diffuse axonal injury

A

Immediate loss of consciousness, remain comatose or enter persistent vegetative state

452
Q

Features of chronic traumatic encephalopathy

A 
Inattention 
Low mood
behaviour change 
Confusion
Memory loss

Eventually, dementia and Parkinsonism

453
Q

Features of Shaken Baby Syndrome (Non accidental head injury)

A

Triad:
Encephalopathy
Subdural haematomas
Retinal haemorrhages

Non specific presentation: hypotonia, listlessness, vomiting, irritability, lethargy.

454
Q

Signs of raised ICP in infants

A 
Irritability 
Failure to thrive 
Sleepiness 
Prominent head veins 
Sunset sign (Parinaud’s Syndrome) - white sclera visible above iris 
Apnoea if brainstem compression
455
Q

Definition of subfalcial herniation

A

Cingulate gyrus moves from one hemisphere to the other, under the falx cerebri

456
Q

Definition of uncal herniation

A

Transtentorial - medial temporal lobe moves from the middle, into the tenotorial opening

457
Q

Signs of uncal herniation

A

Ipsilateral, fixed, dilated pupil (CN III compression)
Ipsilateral cortical blindness (infarct of posterior cerebral artery)
False localising sign i.e. CN VI palsy (paralysis ipsilateral to lesion due to compression of cerebral peduncle)

458
Q

Definition of cerebellar tonsillar herniation

A

Cerebellar tonsils displaced into foramen magnum

459
Q

Presentation of cerebellar tonsillar herniation

A

Stiff neck and head tilt.

Cardiorespiratory arrest due to compression of pons and medulla

460
Q

Traumatic brain injury can result in cerebral oedema.

What is the difference between vasogenic and cytotoxic oedema?

A

Vasogenic - accumulation of water in interstitial CNS spaces due to increased vascular permeability. More likely to involve white matter, and extends along optic nerves → papilloedema.

Cytotoxic - accumulation of water in injured cells.

461
Q

Cervical immobilisation is indicated if:

A 
GCS < 15
Neck pain or tenderness 
Focal neurological deficit 
Paraesthesia in extremities 
Clinical suspicion of cervical spine injury
462
Q

Battle’s sign

A

Post auricular bruising seen in basal skull fracture

463
Q

Indications for CT scan within 8 hours

A

Loss of consciousness or amnesia PLUS:

> 65 yrs OR
History of bleeding or clotting disorders OR
Dangerous mechanism OR
30 mins retrograde amnesia

464
Q

General features of neuro rehabilitation

A

Dimming of lights
Minimal sensory stimulation
Maximum of 2 people per visit

465
Q

Most common primary brain tumours in adults

A

Meningioma
Glioblastoma
Astrocytoma

466
Q

Most common primary brain tumours in children

A

Pilocytic astrocytoma

Medulloblastoma

467
Q

Most common tumours of the spinal cord

A

Schwannoma
Meningioma
Ependymoma

468
Q

Pilocytic astocytoma

A

Most frequent brain tumourin children.

Usually arise from cerebellum, hypothalamus and optic chiasm.

469
Q

Astrocytomas can progress to…

A

Glioblastoma

470
Q

Why is cerebral oedema common in brain tumours?

A

Tumours have a high metabolism, therefore new vessels must form to supply it.
New vessels have no blood-brain barrier, therefore fluid can leak into surrounding tissue.

471
Q

Glioblastoma

A

Most malignant form of glioma, seen in middle aged adults.
Usually affects frontal ad temporal lobes.
Masses are irregular with cavitation and surrounded by large area of oedema.

472
Q

Ependymoma

A

Brain tumour usually intraventricular (4th ventricle)
Can cause hydrocephalus.

Children > adults

473
Q

Choroid plexus tumours

A

Children and young adults
Arise in both lateral and 4th ventricles
Cause hydrocephalus and raised ICP due to blocking CSF pathways and overproduction of CSF.

474
Q

Medulloblastoma

A

Embryonal tumours of the cerebellum (usually posterior vermis)
Can block 4th ventricle and aqueduct causing hydrocephalus.
Usually seen in children < 10 yrs
Rapid growth - present over weeks to months with signs of raised ICP and cerebellar dysfunction

475
Q

Meningioma

A 
CNS tumour arising from arachnoidal cells.
Adults > children 
Women > men (ostrogen receptors)
Usually benign
Can be completely resected
476
Q

Risk factors for meningiomas

A 
Neurofibromatosis Type II
Cranial Irradiation
Environmental irradiation
Post HI
Breast CA
Females of repro age
Exogenous hormones - HRT or COCP
477
Q

Schwannomas

A

CNS tumour arising from cranial and spinal nerve roots, and peripheral nerves.

90% arise from CN VIII nerve root - Acoustic Schwannoma

Displace brain tissue without invading, cause symptoms due to compression.

478
Q

Anatomic Landmark associated with Acoustic Scwannoma

A

Cerebellopontine angle

479
Q

Bilateral acoustic schwannomas are associated with…

A

Neurofibromatosis type II

480
Q

Investigation of choice for suspected acoustic neuroma

A

MRI of cerebellopontine angle

481
Q

Cranial nerves which can be affected in Vestibular/Acoustic Schwannoma inc. symptoms

A

CN VIII - sensorineural hearing loss, vertigo, tinnitus
CN V - absent corneal reflex
CN VII - facial palsy

482
Q

Features of craniopharyngioma

A 
Endocrine abnormality e.g. prolactinoma 
Bitemporal hemianopia (compression of optic chiasm)
Hydrocephalus (compression of 3rd ventricle)
483
Q

Management of craniopharyngioma

A

Compressive, non functioning lesions are surgically removed.
Smaller, functioning lesions are managed surgically (hormone treatment)

484
Q

Type of lymphoma which may affect the CNS

A

Large B cell lymphoma

485
Q

Most common site of metastasis in the CNS

A

Frontal lobe

486
Q

Central Vs Otological vertigo

A

Central - sense of spinning. Associated with MS, posterior stroke, migraine

Otological - sense of floating or tilting. Associated with BPPV, Meniere’s disease

487
Q

Central causes of vertigo

A 
MS
Posterior stroke 
Posterior fossa tumours 
Migraine 
Intracranial SOL
488
Q

Otological causes of vertigo

A

BPPV
Meniere’s disease
Vestibular Neuronitis
Labrynthitis

489
Q

Hoffman’s Sign

A

Hoffmans sign is elicited by flicking the distal phalaynx of the middle finger to cause momentary flexion. A positive result is exaggerated flexion of the terminal phalanyx of the thumb.

Clinical Medicine (9 decks)

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