Neurology Flashcards

1
Q

what is Gower sign and how to conduct it

A

Lay child supine and ask child to stand

- shows proximal muscle weakness - first turn prone then “walk up” legs with the hands

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2
Q

types and causes of tremors

A
  • essential (initiation and maintenance of posture): AD inheritance or thyrotoxicosis, phaeochromocytoma, wilson
  • intention (end of mvt): wilson
  • static (at rest, disappears with mvt): wilson, parkinson, huntington
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3
Q

what is myoclonus

- causes

A
  • Brief, sudden muscle contractions

* Seen in seizure disorders, metabolic disorders, brain infections, brain injury and degenerative conditions

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4
Q

what is chorea

- causes

A
  • Random rapid movements
  • Seen most commonly in cerebral palsy, Sydenham’s chorea, Wilson’s and Huntington’s disease
  • Due to damage to the corpus striatum
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5
Q

what is athetosis

- causes

A
  • Slow writhing movements
  • Seen in cerebral palsy and Wilson’s disease
  • Due to damage to the putamen
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6
Q

what is dystonia

- causes

A
  • Sustained disturbed muscle contraction causing abnormal posturing
  • Seen with certain drugs (anticonvulsants), trauma, infections, and vascular, metabolic and degenerative pathologies
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7
Q

what is hemiballismus

- causes

A
  • Random gross proximal limb flailing

* Due to contralateral subthalamic brain damage

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8
Q

what is tics

- causes

A

• Spasmodic stereotypic involuntary repetitive movements, typically of the facial movements
• Gilles de la Tourette is an inherited form
Associated vocal tics, obsessive-compulsive disorder and attention deficit hyperactivity disorder

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9
Q

how does CN 4 palsy present

A
  • dipopia when looking down and in

- difficulty when walking downstairs

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10
Q

signs of cerebellar dysfunction

A

Truncal ataxia, dysarthric speech, horizontal nystagmus, intention tremor, dysdiadokinesia, dysmetria

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11
Q

secondary causes of headache

A
  • trauma
  • vascular malformation
  • non vasc intracranial malformation
  • substances and withdrawal
  • infection
  • metabolic disorder
  • facial pain (cranium, neck, eyes, ears, nose, sinus, teeth, mouth)
  • cranial neuralgia
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12
Q

triad of hypertensive encephalopathy

A
  • headache
  • seizures
  • visual impairment
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13
Q

cushing triad

A

raised ICP

  • hypertension
  • bradycardia
  • irregular breathing

seen in the terminal stages of acute head injury and may indicate imminent brain herniation

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14
Q

warning signs for headache

A
	First and worst headache
	Signs and symptoms of raised intracranial pressure
	Aggravation by valsalva maneouvre
	Abnormal neurological findings
	Papilloedema
	Chronic progressive headache, with change in behaviour and deteriorating academic performance
	Early morning vomiting
	Headache waking up patient from sleep
	Immunosuppressed patients
	Neurocutaneous syndromes
	Age < 4 years
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15
Q

what is seen on CT for headaches from sinusitis

and what is the tx

A

 Total opacification, mucosal thickening and air-fluid levels are seen on CT/MRI
 Treat with prolonged antibiotics, short-term decongestants and surgical drainage of sinuses – rarely

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16
Q

Precipitiating causes of migraines

A

anxiety, fatigue, mild head trauma, stress, exercise, excitement, travel, menses, some dietary factors and illness.

17
Q

what are childhood periodic syndromes

A

early life expression of genes later expressed as migraine

  • cyclical vomitting syndrome
  • abdominal migraine
  • benign paroxysmal vertigo of childhood
  • benign paroxysmal torticolis
18
Q

Mgx of migraine

A
Non pharm
	Reassurance
	Elimination of trigger factors
	Stress relief/stress management
	Regular diet
	Sufficient sleep
	Biofeedback
	Relaxation techniques
	Counseling

Pharm - abortive
 Single analgesic – NSAIDs, ergotamine compounds, triptans
 Adjunctive – anti-emetics

Pharm - prophylactic
	Cyproheptadine 
	Beta-blockers – propranolol
	Valproate
	Amitriptyline
	Flunarizine
19
Q

When to consider migraine prophylaxis

A

Considered if headaches occur more than four times per month and require substantial medication for relief.

20
Q

Medical problems associated with seizures

A

 Neurocutaneous syndromes (NF-1, TS, S-W)
 Cerebral palsy
 Neurodegenerative syndromes (Rett’s, Lennox-Gastaut)
 Past hx of organic brain disease: brain tumour, head trauma, meningitis/encephalitis/brain abscess
 Inborn errors of metabolism

21
Q

What is epilepsy

A

Epilepsy is recurrent seizures (>2 more than 24 hours apart) unrelated to fever or acute cerebral insult

22
Q

causes of seizures

A
  • Birth or gestational insults
  • Congenital malformations
  • CNS infections
  • Metabolic disorders
  • Trauma and bleeding
  • Degenerative diseases
  • Neoplasms
  • Toxins
23
Q

what are some epilepsy syndromes you know

A
  • infantile spasms
  • lennox-gastaut syndrome
  • childhood absence epilepsy
  • juvenile myoclonic epilepsy
  • benign rolandic epilepsy
24
Q

Infantile spasm

  • age range
  • EEG features
  • associations
  • tx
A

4-6 months onset, boys>girls
EEG: hypsarrhythmias

associated with: tuberous sclerosis; metabolic disease, birth injury e.g. IVH, HIE; postnatal injury e.g. trauma, infections

tx: vigabatrin or steroids

25
Q

What is west syndrome

A

triad of: (i) infantile spasms; (ii) hypsarrhythmias; and (iii) mental retardation

26
Q

What is Lennox -gastaut syndrome

A

electroclinical syndrome:

  • multiple seizure types
  • EEG showing slow spike and wave
27
Q

Childhood absence epilepsy

  • onset age
  • triggers
  • tx
A

onset 3-10 years, girls>boys
induced by hyperventilation, emotion, hunger
tx: valproate, carbamazepine, lamotrigine

28
Q

What is juvenile myoclonic epilepsy

  • onset
  • EEG
  • tx
A

12-16 years, girls>boys
myoclonic jerks, worse in the morning, no loss of consciousness
EEG: shows normal background, 4-6 per sec irregular polyspike and wave discharge pattern. Photosensitivity is a feature

Tx: valproate, lamotrigine

29
Q

Benign rolandic epilepsy

  • prognosis
  • onset
  • features
  • EEG
  • tx
A

GOOD prognosis, will spontaneously resolve in mid teens

onset 2-14 years
features: drooling, abnormal sensations in the mouth; secondary generalisations. 75% occur in sleep, 25% occur on waking

EEG: repetitive spike focus in the Rolandic area (centrotemporal)

Tx: may not need treatment due to spontaneous resolution; carbamazepine may help

30
Q

First aid advice for seizure

A

(i) Lie the child on the side.
(ii) Do not put things in the child’s mouth.
(iii) Move away any nearby objects to avoid hurting himself or herself.
(iv) Have a time plan: if a seizure lasts longer than 5mins, call an ambulance.

31
Q

SE of

  • carbamazepine
  • valproate
A

(i) Carbamazepine – neutropaenia (screen FBC), nystagmus, ataxia
(ii) Valproate – thrombocytopaenia (screen FBC), hepatitis (screen LFT)

32
Q

Causes of status epilepticus

A

 Sudden withdrawal of anticonvulsants in a known epileptic
 Bad epileptic syndrome e.g. West, Lennox-Gastaut Sudden withdrawal of anticonvulsants
 Acute infection (CNS or systemic)
 Acute insult to the brain
 Brain tumour

33
Q

Medications for status epilepticus

A

IV glucose and IV thiamine if hypoglycaemic

IV benzodiazepine (diazepam or lorazepam): 0.25mg/kg at 1mg/min up to 10mg (up to 0.3mg/kg)
OR
Rectal valium if no IV access (<10kg –2.5mg; >10kg – 5mg)

IV Phenytoin 20mg/kg at 1mg/kg/min (up to 30mg/kg)

IV phenobarbital 20mg/kg

if still persist:
GA/ barbiturate coma with EEG monitoring

34
Q

Complications of status epilepticus

A
	Tissue anoxia – cerebral anoxia
	Brain oedema
	Circulatory shock with renal failure
	Respiratory failure
	Acute rhabdomyolysis
	Severe acidosis
	Hyperpyrexia
	Permanent neurological damage (20-50%)
	Death (8-33%)