Nervous system Flashcards

1
Q

Upper motor neuron (UMN) lesion where does weakness develop?

A

Develops in the weaker muscle groups. The extensors in the arms and flexors in the legs.

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2
Q

UMN lesion - where does spactisity develop and how does it manifest?

A

Spasticity develops in the stronger muscle groups (arm flexors and leg extensors). It manifests as increased tone that is velocity-dependent, ie the faster you move the patient’s muscle, the greater the resistance, until it finally gives way (like a ‘clasp-knife’).

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3
Q

UMN lesion muscle wasting

A

Less prominent

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4
Q

UMN lesion reflexes

A
  • There is hyperreflexia: reflexes are brisk
  • Plantars are upgoing (+ve Babinski sign)
  • ± clonus (elicited by rapidly dorsiflexing the foot; ≤3 rhythmic, downward beats of the foot are normal)
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5
Q

UMN lesion fine motor skills

A

Loss of skilled fine finger movements may be greater than expected from the overall grade of weakness.

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6
Q

Where do lower motor neurone (LMN) lesions exist?

A

Anywhere from the anterior horn cells distally, including the nerve roots, plexuses, and peripheral nerves.

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7
Q

LMN lesion pattern of weakness

A

The pattern of weakness corresponds to the muscles supplied by the involved neurons.

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8
Q

LMN lesion muscle wasting

A

Affected muscles show wasting ± fasciculation

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9
Q

LMN lesion tone

A

There is hypotonia/flaccidity: the limb feels soft and floppy, providing little resistance to passive stretch.

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10
Q

LMN lesion reflexes

A

Reflexes are reduced or absent; the plantars remain flexor.

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11
Q

Muscle weakness grading (MRC classification)

A
  • Grade 0 - No muscle contraction
  • Grade 1 - Flicker of contraction
  • Grade 2 -Some active movement
  • Grade 3 - Active movement against gravity
  • Grade 4 - Active movement against resistance
  • Grade5 - Normal power (allowing for age)
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12
Q

Questions to ask about headaches

A
  • Onset
  • Character
  • Frequency
  • Duration
  • Associated features
  • Precipitating cause
  • Drug history
  • Social history
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13
Q

Rapid onset headache differential diagnosis

A
  • Subarachnoid haemorrhage
  • Meningitis
  • Encephalitis
  • Post-coital headache
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14
Q

Symptoms of subarachnoid haemorrhage

A
  • sudden-onset
  • ‘worst ever’ headache
  • often occipital
  • stiff neck
  • focal signs
  • decreased consciousness
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15
Q

Character - tight band

A

Think tension headache

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16
Q

Character - throbbing/pulsatile/lateralising

A

Migraine

17
Q

What do recurring headaches suggest?

A

Headaches that recur tend to be benign.

  • Migraine
  • Cluster headache
  • Trigeminal neuralgia
  • Recurrent meningitis
18
Q

Why is drug history important in headaches?

A

Exclude medication overuse (analgesic rebound) headache: Culprits are mixed analgesics (paracetamol+codeine/opiates), ergotamine, and triptans.

19
Q

Symptoms of cluster headaches

A
  • Rapid-onset of excruciating pain around one eye that may become watery and bloodshot with lid swelling, lacrimation, facial flushing, rhinorrhoea, miosis ± ptosis (20% of attacks)
  • Pain is strictly unilateral and almost always affects the same side
  • It lasts 15–180min, occurs once or twice a day, and is often nocturnal
  • Clusters last 4–12wks and are followed by pain-free periods of months or even 1–2yrs before the next cluster
20
Q

Cluster headache treatment

A
  • Acute
    • give 100% O2 for ~15min via non-rebreathable mask (not if COPD)
    • sumatriptan SC 6mg at onset
  • Preventative
    • avoid triggers
    • corticosteroids (short term only)
    • verapamil
    • lithium