Koma und Bewusstseinsstörung

• Arousal (wakefulness, alertness, or vigilance, Wachheit) is the ability to open the eyes and the presence of sleep/wake cycles.
•  
• Arousal is regulated and depends on the intact function of the Ascending Reticular Activating System (ARAS), a large sub-cortical area of the brain located in the brain-stem, the diencephalon (hypothalamus and thalami), the basal forebrain and the projections to the cerebral cortex.

• Awareness (awareness of self and environment, i.e. the content of consciousness/Aufmerksamkeit)
• the ability to obey commands.
•  intact function of cerebral cortex and its sub-cortical (mainly thalamic) connections.

Somolenz (schläfrig)->Stupor(braucht starken Weckreiz)->Coma(unresponsiveness, patient does not open their eyes, does not follow commands, cannot be aroused, and has no awareness of self or environment)

arousal without signs of awareness, a wakeful unconscious state

Formen: Persistent->1 Monat nach Hirnschädigung noch vorhanden aber evtl.reversibel

Permanent: irreversibel: noch 3 Monate bis 12 Monate nach Ereignis vorhanden

presence of inconsistent but reproducible goal-directed behaviours e.g. response to command, verbalisations, visual pursuit

Schwierig zu diagnostizieren, besonders im IPS-Setting mit Tubus/Tracheostoma...

fluctuating change in consciousness and awareness

• alteration of attention and organisation of thinking
• associated with abnormal sleep–wake cycle
• psychomotor activity
• perceptions (e.g., hallucinations, illusions)
• emotional behaviour

FOUR:

 Full Outline of UnResponsiveness score. Vier Hirnfunktionen werden getestet:

eye response, motor response, brain-stem reflexes, and respiration pattern

Strukturelle Schädigung: direkte Schädigung: vaskulär, Trauma, Raumforderung,Hirndrucksteigerung

Nicht strukturelle Schädigung: toxisch, metabolisch, infektiös

focal neurological deficits (unilaterally dilated, non-reactive pupils, asymmetric motor responses, disconjugate ocular movements)

commonly have reactive pupils and absence of focal neurological deficits

HIV serology (cryptococcal meningitis, toxoplasma encephalitis, primary CNS lymphoma)

immunological work-up and auto-antibodies (e.g. rheumatoid factor, ANF antibodies, anti-DNA antibodies), 

tests for syphilis in blood and spinal fluid

and Borrelia serology

Vitamin B1-Mangel!

Nystagmus/Ophthalmoplegie, Delirium, Gangataxie

Gedächtnisstörung

posterior reversible encephalopathy syndrome (PRES)

usually manifested by headaches, visual disturbances and seizures.

Brain MRI diffusion is diagnostic and shows typical patterns of bilateral hyper-intensities, predominantly in the posterior parieto-occipital regions, but also sometimes involving the brain-stem.

Epilepsie ist eine chronische Krankheit.

imbalance between cerebral excitation and inhibition.

The excitatory neurotransmitters (e.g. glutamate): An excessively rapid hypersynchronous depolarisation, triggered by failed removal of glutamate from the extra-cellular space, can occur in trauma, hypoxia, ischaemia, and hypoglycaemia.

Cerebral inhibition is provided primarily by gamma-aminobutyric acid (GABA). A loss of normal inhibition occurs, for example, during withdrawal or in the presence of GABA antagonists.

Nach Mauro Oddo

• Durch portosystemische Shunts umgehen toxische Substanzen die Leber und reichern sich im Gehirn an.(usually nitrogenous substances from the intestine such as ammonia or short-chain fatty acids and manganese) 
• The neuroinhibitory substance gamma-aminobutyric acid (GABA) accumulates and the actions of benzodiazepine receptor agonists are augmented.
• The plasma levels of endogenous opiates are increased

disturbed cholinergic activity.

Delirium is a fluctuating alteration of level of awareness with reduced ability to direct, focus, sustain and shift attention.

It is also associated with altered organisation of thinking.

Noteworthy, it is infrequently associated with agitation.

•  absence of a pupillary reaction to light
• a motor response no better than extensor posturing to noxious stimuli
• and the absence of corneal reflexes at day 3 after arrest

• unreactive EEG background was incompatible with good long-term neurological recoveryand was strongly associated with in-hospital mortality.
• presence of at least two independent predictors from the following:
  • incomplete brain-stem reflexes
  • myoclonus
  • unreactive EEG
  • absent cortical SSEP (somatosensory evoked potentials)

post-anoxic myoclonus->responds well to specific treatment

myoclonic status epilepticus -> poor outcome, post-anoxic myoclonus