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Neurology Year 3- K > Common neurological Sx > Flashcards

Common neurological Sx Flashcards

1
Q

Headache

A

Common, usually not serious.
Causes:
Acute severe- onset mins or hours
Intracranial haemorrghage, cerebral Venous thrombosis, Dissection of the carotids/verterobasilar arteries, Meningitis, Head trauma, Migraine, Drugs- GTN, Alcohol, infx- malaria.

Subacute onset- days to weeks
Intracranial mass lesion, encephalitis, meningitis, sinusitis, acute glaucoma, Malignant HTN, giant cell arteritis.

Recurrent/chronic
Migraine
Tension headache (H) 
Sinusitis
Cluster headaches
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2
Q

Causes for H

A

All depends on pressure.
Elderly- pressure on sinus eg turning head.
Postural HTN, systolic >20, sitting to standing after 2mins- in those w/ impaired autonomic reflexes- autonomic neuropathies

+

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3
Q

What drugs predispose to autonomic neuropathies?

A

Phenothiazines

Tricyclic antidepressents

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4
Q

When is tilt table testing performed?

A

To inv syncope in whom cardiac or epileptic causes have been excluded. ECG, BP, HR, recorded after head tilt for 10-60mins.
Re-inteoduction of sx and HTN = +ve test

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5
Q

Whats Narcolepsy? Whats Cataplexy?

A

Rare disorder - periods of irriversible sleep in inappropriate circumstances.
Cataplexy- related cx- which sudden loss of tone develops in lower limbs with oreservation of consiousness.
Attacks are set off by suudden suprise or emotion.

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6
Q

Weakness

A

Skeletal muscle controlled by motor axis in CNs.
Muscle weakness -> defect in:
1. Motor cortex
2. Corticospinal tract- Pyramidal system
3. Anterior horn cells- cross over in medulla as halves lateral corticospn tracts
4. Spinal nerve roots
5. Peripheral nerves
6. Neuromascular junction
7. Nerve fibers

True weakness or tirdness or slowiness like in Parkinsons (PD)

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7
Q

Comparison: lesions in the cosrticospinal tract of UMNL

A 
UMNL- signs on opposite site of lesion
NO fasciculations
NO muscle wasting
⬆️ spasticity +\- clonus
Weakness in extensors in arms and flexors in legs

⬆️⬆️ exaggerated tendon reflexes
Extensor plantar response
Drift to outstretched hand ( downwards, medially with tendency to pronate)

Acute injury to UMN can H/w be manifested by transient ‼️ flaccid weakness and hypoflexia.

Inv- MRI/CT

Hemiparesis and Paraparesis
Hemiparesis: 1 side weak limbs- usually lesion in brain or brainstem- stroke
Parapaesis- Weak legs 2! -> bilateral damage since halves cross.
Usually lesion in SC below T1 ❌‼️

Tetraparesis
- quadriplegic- weakness of arms and legs-> high cervical cord damage- trauma usually.

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8
Q

LMNL

A

Signs on same side as lesion (makes sense, its lower, it has already crossed over !)
Fasciculation (visible contraction on single motor units (makes sense- individual damaged neural fibers sent directly wrong action potentials that are correctly read)
Wasting (makes sense- the damaged neurones that are responsible ↪️for specific muscle fibers do not stimulate them to “grow”)
↪️Hypotonia
↪️Weakness
Loss of tendon relfexes ‼️

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9
Q

Lesion- what happens?

A

UMN signs below lesion, LMN signs at level of lesion,

Unaffected muscles above the lesion.

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10
Q

Acute onset H

What F suggest subarachnoid haemorrhage?

A
  1. Reaches max intensity in secs or mins
  2. Rapid onest after exercise strenous
  3. Worst ever H
  4. Never b4
  5. Change in level of consciousness
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11
Q

What indicates meningeal irritation?

A

Neck stiffness and + ve Kernig’s sign

  1. B meningotis
  2. V meningitis
  3. Subarachn haem.

Fever may also occur with these.
Hx Key- to chronic recurrent H( tension type) -> no further invx.

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12
Q

What may be due to ⬆️ICP?

A

Worsening H or chroning w/ chaning character-> eg due to mass- space occupying lesion -CT/MRI

Others:

  1. H when waking up in morninh that improves w/ sitting up
  2. H assc w/ N+V (CTZ) may also occur w/ migraine
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13
Q

What sx indicate a serious cause?

A

Ataxia
Neuro deficit
Papiloedema
Altered mental status

Require brain imaginh

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14
Q

What suggests giant cell arteritis?

A

H w/ generalised aches and pains in elderly

‼️ urgent tx w/ steroids to prevent blindness.

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15
Q

What are some common causes of attacks of altered consciousness and falls in adults?

A 
Syncope - 1. Simple faint. 2. Cough - 3. Effort, 4. Micturition.
Carotid sinus 
Cardiac arythmias
Postural HTN
Epilepsy
Hypoglycaemia 
TIA
Psychogenic attacks- panic attacks, Hyperventilation
Narcolepsy + cataplexy

Differantiation- medical hx

Severe cough- obstructing venous return to ❤️
Effort- exercise in pts w/ aortic stenosis + hypertrophic obstructive cardiomyopathy.
Carotid sinus syncope: Xs sensitivity of sinus to external pressure. May be on elderly like tilting head.

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16
Q

Dizziness + syncope

A

Syncope: temporary impairment of consciousness due to reduction in cerebral blood flow- recovery is rapid + complete.

Dizziness- or faintness preceeds syncope- incomplete form in which cerebral perfusiom not fallen suffeciently to cause loss of consiousness. ❌ Not vertigo.

Most common cause of Dizzinesns- vasovagal syncope- simple faint- due to reflex braducardia and peripheral + splanchnic vasodilation (causing brady)
- Fear, Pain, prolonged standing !

17
Q

Whats vertigo?

A

Illusion of rotatory movement- pt feels that surroundings are spinning

Disease of inner ear- 8th Cranial nerve or its central connections.

18
Q

What usually preceeds a faint?

What differentiates it from a fit?

A

Nausea, swating, lightheadedness, pallor.
Diff/
Rapid recover w/o urinary incontinence, jerking movements .
H/w loss of consciousness due to arrythmia occurs w/o warning❗️ Even in supine pstn.

19
Q

What might cause syncope in men esp at night?🌙✨

A

After Micturition ! Esp at night.

+ When venous return to heart is obstructed by breath holding attacks and severe coughing.

20
Q

Numbness

A

Sensory-> DRG (ganglion) -> cord-> thalamus-> cerebral columns in 2 paths:
1. Posterior columns- vibration, joint position (proprioception) , light touch. 1o-> uncrossed through in gracilis + cuneate nuclei in medulla. 2o-> cross to form medial lemniscus -> thalamus.

  1. Spinothalamic - Pain + temp .
    Synapse at Dorsal Horn , cross midline + -> ascend in spinothalamic tract. To thalamus.

Paraethesis- pins + needles, numbness + pain - principal sx of sensoty lesions below level of thalamus.

21
Q

Peripheral nerve lesions

A

Sc felt in distribution of affected nerve- eg ulnar + median nerve.
Polyneuropathy- bilateral symmetrical , distal sensory loss + burning.

22
Q

Spinal root lesions

A

Sx referred to dermatome - tingling discomfort.

While sensory tracts lesion- defect in extremity rather than specific dermatomes.

23
Q

Spinal cord lesions

A

Sx e.g loss of sx, below lesion.
Spinothalamic lesion whether in brain or SC- loss of contralateral pain + temp (cz cross at spinal level) below lesion.

Lesion at posterior columns- loss of sensations ipsilaterally below lesion.

24
Q

Pontine lesions

A

Pons lie above decussation of posterior columns.
Medial lemniscus + spinothalamic tract- close together, so
LOSS OF ALL FORMS OF SENSATION ON OPPOSITE SITE.

25
Q

Thalamic lesions

A

Rare cause of complete contralateral sensory loss.

Pain due to infract as well.

26
Q

Cortical lesions

A

Parietel cortex

No pain

27
Q

Reflexes and root values

A 
Ankle jerk T1
Knee jerks L2,3,4
Biceps jerks C5- 
Supinator jerk C6
Triceps jerks C7
Abdominalis T8-11
28
Q

Tremor

A

Rhythmic involuntary muscular contraction.
Resting tremor- PD, parkinsonism, Wilsons.

Postural tremor- when pt attempts a posture eg outstrech hands (UMN?)- psychological- due to ⬆️ symp activity.
Some PD + cerebellar d.

29
Q

Intention tremor

A

Occurs during voluntary movement + gets worse when approxhing the target- finger to nose testing, + cerebellar d.

30
Q

Task specific tremor

A

Appears when oerforminh goal orientated tasks - hand writing, speaking, standing.

Inv- TSHs- wilsons d-

31
Q

What happens in VitB12 deficiency?

A

Causes a syndrome of subacute combined degeneration of the cord.
Distal sensory loss (esp posterior column)
Absent knee jerks (due to neuropathy)
And evidence of cord disease (⬆️⬆️ knee jerk reflexes, extensor plantar response)-UMN.

Tx/ IM vitB12 -> revereses the peripheral nerve damage but little effect on CNS.

32
Q

What is respomsible for movement coordination?

A

Extrapyramidal system + cerebellum- dx- no muscular weakness, but incoordination.,

33
Q

Myopathies

A

Myopathies (duchennes) are proximal (except myotonic dystrophy
Peripheral neuropathies ate distal excpr GBS.

34
Q

What happens when the cerebellum is affected?

A

Each lateral cerebellum- resp for ipsilateral limb.

Midline vermis- midline- axial balance and posture.

35
Q

What are some causes of cerebellar lesions?

A

MS
Space occupying lesions: 1o tumour- medduloblastoma,2o, abscess, haem.

Chronic alcohol abuse
ANticonvolusants,
Spinocerebellar ataxia, dominantly inherited, rare.

36
Q

What sx will a lesion in 1 cerebellar lobe give?

A

Ataxic gait + broad base, pt falters in lesion side.
An intention tremor - PD compare- w / past pointing.
3. Dysdiadochokinesis- clumsy rapid alternating movements- e.g. Tapping hand on back of other.
4. Horizontal nystagmus- fast component at lesion side.
5. Dysarthria- usually w/ bilateral lesions- scanning speech, halting jerking
6. Titubation (rhythmic head tremor) , hypotonia, depressed redlexes. No muscle weakness.

37
Q

What sx will lesions in the cerebellar vermis produce?

A

Ataxia of trunk,

So hard to sitt up or standing.

Neurology Year 3- K (14 decks)

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