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
what physiological signs could indicate tectorial herniation of the brainstem (coning)
increasing blood pressure and declining heart rate
26
what is an eye sign that could indicate raised ICP/uncal herniation
CN third nerve palsy - ptosis - dilated pupil - pupil down and out
27
what are false localising signs, give examples
signs of raised ICP ipsilateral to pressure third and sixth nerve palsy
28
what are true localising sings, give an example
signs of raised ICP contralateral to pressure hemiparesis
29
what is an extradural haematoma and where does it most commonly occur
arterial bleeding secondary to trauma typical from the middle meningeal artery - corresponds to weakest part of the skull (temporal bone)
30
what are some risk factors for intracranial haematoma
skull fracture | altered consciousness
31
what are the different types of head injury that can lead to focal neurological sings and/or seizures
diffuse axonal injury contusion ICH/IPH ECH - extradural, subdural
32
what is the management of a head injury
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
how is raised ICP treated
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
what drugs are NOT useful in treating raised ICP from a bleed
steroids - will work for tumour swelling but not osmotic swelling
35
how do subdural and extradural haematomas differ on CT
subdural - ellipse shape (curves along edge, think banana) extradural - lens shape (curves in, almost oval)
36
how is a subdural haematoma caused
from a head injury causing shearing forces in the bridging veins between the dura and arachnoid
37
how can subdural haematomas present
can be acute, subacute or chronic typically delayed symptoms following trauma due to slow venous bleeding
38
what are the risk factors for subdural haematoma
elderly/dementai/alcoholics - anything causing brain atrophy aspirin and warfarin
39
what are the two components of consciousness
1. arousal (reticular activating system, pons) | 2. awareness of environment (cerebral hemispheres)
40
what are the decreasing states of consciousness
lethargy stupurous obtunded coma
41
how does locked in syndrome occur
damage to the brainstem, very commonly the pons
42
what are the features o flocked in syndrome
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
list some common causes ov a low GCS
Hypoxia / hypercapnia / sepsis / hypotension Drug intoxication / renal or liver failure Hypoglycaemia, ketoacidosis Seizures Causes of raised intracranial pressure tumour, stroke, EDH, SDH, SAH, hydrocephalus