1. Disorders affecting consciousness Flashcards

1
Q

what are the two groups of disorders that affect consciousness

A

episodic loss (or alteration) of consciousness

persistent alteration of consciousness

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2
Q

give some examples of episodic loss/alteration of consciousness

A

seizure
syncope (vasovagal/cardiogenic)
non-epileptic attack (pseudoseizure, dissociative attack)

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3
Q

give some examples of causes of persistent alteration of consciousness

A

encephalopathy - “brain dysfunction”
encephalitis - “brain infection or inflammation”
raised ICP

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4
Q

what are the clinical features of a seizure

use:
triggers
preceding symptoms
blanks
fall
ictus
duration
post-ictal
A

triggers - rare

preceding symptoms - sensoral, psychic, tomato-sensory, auras, motor

blanks - dissconection or abrupt loss

fall - fast, tonic

ictus - tonic clonic, tonic

duration - GTCS 30s-5m, Secondarily GTCS ~62s

post-ictal - confusion, somnolence, headache

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5
Q

what are the clinical features of syncope

use:
triggers
preceding symptoms
blanks
fall
ictus
duration
post-ictal
A

triggers - frequent

preceding symptoms - N/V, visual blurring, epigastric pain, heat, headache, tinnitus

blanks - fading away

fall - slow, flacid

ictus - flaccid, tonic anoxic seizure

duration - ~15s (3-30s)

post-ictal - somnolence, headache

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6
Q

what are the clinical features of a non-epileptic attack

use:
triggers
preceding symptoms
blanks
fall
ictus
duration
post-ictal
A

triggers - stressful situation (but may be none)

preceding symptoms - hyperventialtion, panic, none

blanks - variable

fall - variable

ictus - motionless, variable thrashing movements

duration - usually >5mins, often much longer

post-ictal - variable

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7
Q

what are the two groups of seizures

A

focal

primary generalised

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8
Q

what are the three types of focal seizures

A

simple partial - no loss of awareness

complex partial - loss of awareness

secondary generalised - focal that spread resulting in a tonic clonic seizure

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9
Q

what are the three types of primary generalised seizures

A

tonic-clonic
absences
myoclonic

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10
Q

what is the definition of epilepsy

A

more than one seizure

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11
Q

what is the lifetime prevalence of any seizure compared to % of people with epilepsy

A

lifetime prevalence of any seizure = 1-2%

epilepsy = 0.5-1%

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12
Q

what are risk factors for epilepsy

A

Family history

Focal brain damage / pathology
e.g. stroke, tumour, meningitis, trauma, learning difficulty

Toxins, drug withdrawal, infection, metabolic disturbance (e.g. hypoglycaemia)

Sleep derivation

All LOWER SEIZURE THRESHOLD

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13
Q

what is important to know when making a diagnosis of epilepsy

A

GOOD HISTORY

From patient and eye witness
- before the attack, prodrome, during the attack, after the attack

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14
Q

what investigations can be done for epilepsy

A
MRI (gold standard)
CT
EEG
ECG
routine bloods
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15
Q

what is the treatment for epilepsy

A

Treat risk factors if possible e.g. reduce / stop alcohol

Usually drug therapy if > 1 seizure

  • 2/3rds with epilepsy respond well to treatment
  • 1/3rd more difficult and resistant to treatment
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16
Q

what are some common drugs used in epilepsy

A

Sodium valproate (Epilim)**
Carbamazepine (Tegretol)
Lamotrigine

Phenytoin**

Leviteracetam **
Topiramate
Gabapentin / Pregabalin

Phenobarbitone

**available for IV use

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17
Q

what is the Glasgow coma scale

A

GCS used to assess consciousness in a patient

scored from 3-15 over 3 areas - eye opening, verbal response, motor response

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18
Q

what is the scoring for eye opening in the GCS

A

4 - spontaneous
3 - to speech
2 - to pain
1 - none

19
Q

what is the scoring for verbal response in the GCS

A
5 - orientated
4 - confused
3 - inappropriate
2 - incomprehensible
1 - none
20
Q

what is the scoring for motor response in the GCS

A
6 - obeys commands
5 - localises to pain
4 - withdraws from pain
3 - flexion to pain
2 - extension to pain
1 - none
21
Q

what are flexion and extension to pain also known as and what does this indicate

A

flexion = decorticate rigidity/posturing
- indicates there may be damage to the cerebral hemispheres, internal capsule, thalamus and potentially midbrain

extension = decerebrate rigidity/posturing
- indicates brainstem damage (below the red-nucleus) damage to the midbrain (worse than decorticate) and damage to the cerebellum

22
Q

what is transition of flexion to pain (decorticate) to extension to pain (decerebrate) indicative of

A

uncal (transtentorial) or tonsilar brain herniation

23
Q

what are the different ways of assessing conscious level

A

observation (spontaneous movement, seizure like activity)
GCS
brainstem reflexes

Review all other causes of low GCS, temp, BP, HR, cardiovascular, respiratory (O2, CO2), drugs, toxins

*think - could patient be conscious but paralysed?

24
Q

what are the key brainstem reflexes to loom for in assessing patient consciousness

A

Pupillary light reactions (CN II+III)

Doll’s eye movement (IV, VI and VIII)

Corneal reflex (V + VII)

If intubated, gentle tugging on endo-tracheal tube

25
Q

what physiological signs could indicate tectorial herniation of the brainstem (coning)

A

increasing blood pressure and declining heart rate

26
Q

what is an eye sign that could indicate raised ICP/uncal herniation

A

CN third nerve palsy

  • ptosis
  • dilated pupil
  • pupil down and out
27
Q

what are false localising signs, give examples

A

signs of raised ICP ipsilateral to pressure

third and sixth nerve palsy

28
Q

what are true localising sings, give an example

A

signs of raised ICP contralateral to pressure

hemiparesis

29
Q

what is an extradural haematoma and where does it most commonly occur

A

arterial bleeding secondary to trauma

typical from the middle meningeal artery - corresponds to weakest part of the skull (temporal bone)

30
Q

what are some risk factors for intracranial haematoma

A

skull fracture

altered consciousness

31
Q

what are the different types of head injury that can lead to focal neurological sings and/or seizures

A

diffuse axonal injury
contusion
ICH/IPH
ECH - extradural, subdural

32
Q

what is the management of a head injury

A

Stabilise cervical spine

ABC: Airway/Breathing/Circulation

If GCS<8 – intubation + ventilation

Treat raised ICP

Cranial imaging- may need decompressive surgery or removal of haematoma

Neuro observation (GCS)

33
Q

how is raised ICP treated

A

Surgery to relieve pressure
heamatoma, ventricular shunt

Osmotic agents e.g. mannitol

Nurse with head at 30-45% (Venous return)

Reduce pain

Maintain good PO2, reduce PCO2

Reduce metabolism (reduce temperature, barbiturates eg thyopentone) - help brain recover

34
Q

what drugs are NOT useful in treating raised ICP from a bleed

A

steroids - will work for tumour swelling but not osmotic swelling

35
Q

how do subdural and extradural haematomas differ on CT

A

subdural - ellipse shape (curves along edge, think banana)

extradural - lens shape (curves in, almost oval)

36
Q

how is a subdural haematoma caused

A

from a head injury causing shearing forces in the bridging veins between the dura and arachnoid

37
Q

how can subdural haematomas present

A

can be acute, subacute or chronic

typically delayed symptoms following trauma due to slow venous bleeding

38
Q

what are the risk factors for subdural haematoma

A

elderly/dementai/alcoholics - anything causing brain atrophy

aspirin and warfarin

39
Q

what are the two components of consciousness

A
  1. arousal (reticular activating system, pons)

2. awareness of environment (cerebral hemispheres)

40
Q

what are the decreasing states of consciousness

A

lethargy
stupurous
obtunded
coma

41
Q

how does locked in syndrome occur

A

damage to the brainstem, very commonly the pons

42
Q

what are the features o flocked in syndrome

A

patient is fully conscious and aware however they are completely paralysed apart from blinking and vertical eye movement (midline functions so preserved)
- everything below the pons doesn’t work

43
Q

list some common causes ov a low GCS

A

Hypoxia / hypercapnia / sepsis / hypotension

Drug intoxication / renal or liver failure

Hypoglycaemia, ketoacidosis

Seizures

Causes of raised intracranial pressure
tumour, stroke, EDH, SDH, SAH, hydrocephalus