Neuro - Coma

Front 1

Somnolence

Back 1

Sleep

Front 2

Stupor

Back 2

Briefly arousable

Front 3

Coma

Back 3

Unarousable

Front 4

Sleep

Back 4

Arousable, fluctuates

Front 5

Reticular Activating System

Back 5

Pontocortical afferent system.

Tegmentum of brainstem (abova pons) and paramedian thalamus (above that)

Bilateral interruption required to reduce consciousness.

Front 6

Things that can cause coma

Back 6

Lesion in...brainstem, bilateral cerebrum, or diffuse CNS compromise.

Front 7

Supratentorial mass - general pathophys

Back 7

TO cause coma, must either cause dysfunction of upper portions of RAS bilaterally

or produce downward herniation of the brain to compress the brainstem RAS.

Caused by hemorrhage, tumor, abscess, hydrocephalus

Front 8

Divisions of supratentorial mass lesions

Back 8

Subfalcine herniation - Causing massive pressure. (entire cerebral hemisphere is moved laterally)

Transtentorial herniation - Temporal lobe or diencephalon moves down to compress brainstem.
1. Uncal - e.g. subdural hematoma or temporal mass - medial part of the temporal lobe
2. Central - e.g. thalamic hemorrhage.

Front 9

Uncal transtentorial herniation

Back 9

e.g. subdural hematoma or temporal mass

Supratentorial mass lesion

Medial temporal lobe 1.compresses CNIII causing ipsilateral pupil dilatation and poor EOMs.
2. ipsilateral hemiparesis due to compression of midbrain peduncle by Kernohan's notch of tentorium,
3. Cheyne Stokes or hyperventilation
4. Posturing (rigidity and strange body positioning - means you are disinhibiting some reflexes)
5. Bilateral fixed pupils, death

Front 10

Central transtentorial herniation

Back 10

e.g. thalamic hemorrhage

symmetrical.

Early coma (bc early brainstem compression), small pupils, normal EOMs, posturing, later on becomes similar to uncal herniation.

No third nerve palsy early on.

Front 11

Infratentorial mass lesions with compression or insult to the brainstem.

Back 11

Basic mech - mass compressing brainstem.

Examples are hemorrhage and big strokes

1. Bilat motor or sens loss
2. Often crossed syndromes (e.g. weakness of face on left and body on right - this is common with brainstem lesions)
3. miosis (think Horner's)
4. loss of lateral gaze with preserved vertical gaze
5. Abnormal resp including cheyne stokes respiration.

Front 12

Diffuse/multifocal brain disease

Back 12

Basic mech - diffuse damage to RAS or increased ICP

1. early resp dysfunction (when severe)
2. myoclonus (brief invol twitching of muscles)
3. posturing
4. REACTIVE PUPILS!

Front 13

DDx of diffuse/multifocal brain disease

Back 13

CVA, vasculitis, central venous thrombosis, subarachnoid hem, ischemia, infection (meningitis/enceph), toxins, hypoglycemia

Front 14

Clue of supratentorial lesion

Back 14

If via herniation syndrome, usually get a coma before any brainstem signs.

Front 15

Clue of infratentorial lesion

Back 15

First get cranial nerve signs then coma.

Front 16

Clue of metabolic coma

Back 16

Preserved pupillary reflexes even after respiratory and eye movement function is lost.

Front 17

Locked in syndrome

Back 17

Total paralysis of limbs and most cranial nerve.

NOT A COMA!

Must distinguish by seeing vertical eye movement or EEG.

e.g. pts with brainstem stroke, CPM, guillain-barre syndrome, ALS

they can hear things at the bedside!!!

Front 18

Vegetative state

Back 18

Destruction of most of the cerebrum with intact brainstem and thalamus/hypothal (ddx is anoxia or multiple CVAs)

Patient is only reflexive.

This is not a minimally conscious state bc pt can not wake up from this.

Front 19

Akinetic mutism

Back 19

Pt is responsive but very slow (abulia).

Lesion is frontal or medial thalamic

Patients generally appear awake but occasionally appear unconscious.

Front 20

Psychogenic coma

Back 20

Catatonia (hold rigid poses for hours. pt may respond to)) vs. hysterical coma (dissociative disorder - a manifestation of conversion disorder - ignoring the pt tends to help)

both have normal EEG. sodium amytal helps both.

Front 21

Causes of cheyne stokes

Back 21

Metabolic encephalopathy, increased ICP, bilateral cerebral insult, upper brainstem lesion.

Front 22

Hyperventilation causes

Back 22

metabolic acidosis, rostral brainstem.

Front 23

Apneustic

Back 23

Inspiratory pauses (lesion in pons)

Front 24

Ataxic breathing pattern

Back 24

Disorganized - due to lesion in medulla.

Front 25

Causes of enlarged pupils

Back 25

Parasymp or CNIII lesion

If bilateral, might be parasym meds, barbituate intox, postictal state (period after a seizure)

Front 26

Contricted pupil causes

Back 26

Sympathetic lesion (hypothalamus or carotid)

Front 27

Pinpoint pupil causes

Back 27

Pons or opioids

Front 28

Midposition unreactive pupil causes

Back 28

Symp and parasymp lesions. Usually a very bad sign. (usually a midbrain lesion)

Front 29

EOMs

Back 29

Doll=eyes maneuvers (if cervical spine is stable) or cold water nystagmus.

Front 30

Decorticate posturing

Back 30

Better to have this kind.

arm adducted, elbow/wrist flexed, fist clenches, hip and knee extended

lesion of corticospinal tract in deep hemisphere or upper midbrain.

Front 31

Decerebrate posturing

Back 31

Worse to have this kind.

arm adducted, elbow extended, wrist flexed, hip and knee extended, toes pointed.

lesion in low midbrain or below.

Front 32

Treatment steps in pt with coma

Back 32

Stop hemorrhage, ABCs, monitor for arrythmias.

Labs (glucose, lytes, BUN, cr, LFTs, CBC, ESR (eryth sed rate), ABG, tox screen

Tx with thiamine and naloxone

LP, history, CT, MRI, EEG, ECG.

Front 33

Indic for intubation

Back 33

Resp distress, hypoxemia, hypercarbia, risk of aspiration

Front 34

Determinants of cerebral blood flow

Back 34

BP and ICP.

If ICP stays > 18cm, need serious intervention.

Front 35

Cushing reflex

Back 35

MAP is less than ICP, so sympathetic stim to increase BP. This triggers vagal response to decrease pulse. And the compression of the brainstem causes a decreased RR.

Front 36

Tx of increased ICP

Back 36

Hypervent, diuretics, sedatives, steroids, craniotomy, shunt.

Front 37

Cerebral hypoxia - Injures what first?

Back 37

Most metab active - basal ganglia, hippocampi, cerebral cortex.

Front 38

Central pontine myelinolysis

Back 38

Technically an infrantentorial mass lesion.

Demyelination of central portions of the pons from rapid correction of hyponatremia.

Also seen in pts with nutritional deficiencies.

Clinically presents as minor motor/sensory deficits to quadriplegia, locked in syndrome and coma. Delerium is common.

Usually lag of 1-2 days btwn shift in sodium and presentation of CPM symptoms.

Front 39

Things not to miss!

Back 39

Hemorrhages (intracerebral or subarachnoid)
Mass
Meningitis/Encephalitis
Seizure
Trauma (subdural hematoma), contusions
metabolic causes
drugs (intox, withdrawal, iatrogenic)

Front 40

Things required for consciousness

Back 40

RAS (upper pons through midbrain - paramedian region), diencephalon (thalamus), cerebral hemispheres.

Front 41

Brain death criteria

Back 41

1. Deep coma - no response to stimulus

2. Severe brain stem damage - demonstrated by absent pupillary light rxn and loss of VOReflex and corneal reflex.

3. absence of function of medulla manifested by complete apnea even when pCO2 is high.

Front 42

Cluster breathing

Back 42

No crescendo-decresendo pattern (like in CSBreathing) but apneic spells and then hyperventilation.

Front 43

Kussmaul breathing

Back 43

Deep hypervent - indicates metabolic acidosis or upper brainstem lesion.

Front 44

Agonal gasps

Back 44

Lower brainstem (medullary) damage

Front 45

Anisocoria - which eye is bad?

Back 45

If large pupil is abnormal - should fail to constrict to light.

If small is abnormal - should fail to dilate to dark.

Front 46

Uncus

Back 46

Medial temporal lobe.