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Hendro BIrowo
CONSCIOUSNESS
Component of conciousness
Conciousness has two mayor components
Anatomy of consciousness
The ARAS and Essential Neurotransmitters
Locus Coeruleus: Epinephrine
Raphe Nucleus: Serotonin
Basal Nucleus: Acetylcholine
A summary diagram of the ascending arousal system
Yellow : cholinergic system
Red :The cortex is activated simultaneously by a series of direct input include monoamine inputs from the upper brainstem and posterior hypothalamus.
1.NA from LC2.Serotonin from the dorsal and me dian RN3.DA from ventral periacque. Gray matter4.His from TMN5.ORX and MCH from Lat Hypothal6.Ach and GABA from the Basal Fo rebrain
Disorders of Consciousness
Disorders of Consciousness
Disorders of Consciousness
Qualitative level of conciousness
Quantitative level of conc.Glasgow Coma Scale (GCS)
Eye response
Eyes open spontaneously = 4Eye opening to verbal command = 3Eye opening to pain = 2No eye open = 1
Motor response
Obeys command = 6 Localizing pain = 5 Withdrawal from pain = 4 Flexien response to pain = 3 Extension response to pain = 2 No motor response = 1
Verbal response
Oriented = 5 Confuse = 4 Inappropriate word
= 3 Incomprehensible sound =
2 No verbal response = 1
Etiologies of loss of consciousness (coma).
Differential Diagnosis of ComaDisorder Distinguishing clinical feature Making the diagnosis
Stroke • Acute onset
• Neurological deficit
•Clinical diagnosis of coma and sign of severe brain damage in focal distribution approriate to the coma
•Imaging : infarct or haemorrhage
Anoxia • Coma following episode of anoxia
• Myoclonus and/or seizure are often seen
• Multifocal sign with unequal region of anoxic
• History of cardiac arrest or other cause of anoxia
•Clinical feature of coma with or without myoclonus
Intoxication • Coma with lost of brainstem reflexes without other focal sign
• History of substance ingestion
• Clinical feature are nonspecific. Suspicion is key
• Drug screen is critical
Differential Diagnosis of ComaDisorder Distinguishing clinical feature Making the diagnosis
Head injury • Coma following head injury with
or without focal sign
• Mental status fluctuate with
cerebral edema and other factor
• Overts sign of injury are present
• Clinical feature
• History of head injury
• Imaging : normal, contusion,
edema, haemorrhage
Metabolic derangements
• Metabolic derangements are
uncommon cause of coma, more
often encephalopathy
• Coma with preserved brainstem
function can be seen. Seizure can
occur
• Lab results show
abnormality : electrolytes,
etc.
• Imaging and lab result do
not show other cause –
consider another causes
Locked in syndrome in
brainstem infarction
• Patient imobile, on casual
observation appear to be comatose
• Patient retain vertical eye
movement and communication is
possible with this condition
• Able to communicate with
eye movement
• Brainstem infarction may see
in MRI or CT
Differential Diagnosis of ComaDisorder Distinguishing clinical feature Making the diagnosis
Pseudocoma • Clinical appearance of coma with preservation of brain function
• Patient may be unaware of the pseudocoma or be intentionally unresponsiveness
• Evidence of exam of preserved response :
• Hold arm over head and let it fall-
Metabolic derangements
• Metabolic derangements are
uncommon cause of coma, more
often encephalopathy
• Coma with preserved brainstem
function can be seen. Seizure can
occur
• Lab results show
abnormality : electrolytes,
etc.
• Imaging and lab result do
not show other cause –
consider another causes
Approach to the diagnosis of the unconscious patient Determine rapidly the cause of the impairment the structural or metabolic and what treatment
The key component of the examine include the level of conc, the pattern of breathing, the size and the reactivity of the pupils, the eye movement and oculovestibular response
Diagnosis
Evaluation is aimed at: Characterizing the nature of the disorder: ACS,
Dementia Determining cause
History: HPI: History of Present Illness PMH: Past Medical History
Cardiovascular Disorders – level & content Diabetes - content Head Trauma – level & content Alcoholism - content
FH: Family History SH: Social History
Respiratory patterns yields information regarding the activity of different cerebral areas
Pupil (size in mm) in ambient light, and in reaction to direct/consensual light.
Pupillary Responses in Various Lesions
Signs of increased ICP/Herniation
PupilsUnilateral dilated pupil Bilateral small poorly reactive pupils
Eye movementsThird nerve palsySixth nerve palsyCan be assessed by cold caloric
FundoscopySigns of papilledema?
Respiratory pattern?
Herniation syndromes.
The most common causes of herniations of the brain are : The mass effect increases the intracranial pressure
and causes internal shifts or herniations of the brain that compress the normal tissue, in particular the diencephalons and brainstem.
This compression impairs consciousness and the life-sustaining functions of breathing, blood pressure control, and temperatur regulation.
Herniations also compress cerebral arteries resulting in infarctions.
Etiology : Cerebral contusions, hematomas, abscesses,
neoplasms, cerebral edema.
Trans facial herniation. The part of the hemisphere that shifts under the falx
is called the cingulate gyrus. It may compress the artery against the free edge of
the falx, causing infarction of medial hemispheric wall dorsal to the corpus callosum. This infarction would cause UMN paralysis of the leg.
Uncal herniation (trans tentorial herniation ) Occurs in rapidly expanding traumatic hematomas Frequently in the lateral middle fossa or temporal
lobe pushing medial uncus and hippocampal gyrus(uncal herniation) over edge of tentorium (tentorial herniation), entrapping third nerve and directly compressing midbrain.
Impaired conscousness is not a reliable early sign. Earliest consistent sign : unilateraly dilating pupil
Trans foraminal herniation. Herniation of the intracranial contents caudally, the
cerebellum and medulla into the foramen magnum. May result from expanding supratentorial lesions or
from expanding infatentorial lesions, such as cerebellar hemorrhage or neoplasm.
Infratentorial masses also may cause upward transtentorial herniation, causing midbrain compression and midbrain sign.
Clinical syndrome of transforaminal herniation : Quadriplegia. Apnea compression of reticulospinal tracts that stop
automatic breathing.
April 2007
Critical damage to the reticular system produces coma, a pathological state of eyes-closed unresponsiveness in which the patient lacks both wakefulness and awareness
Critical damage to the thalami, cerebral cortex, or its connections, while sparing the reticular system, produces the vegetative state, in which the patient is awake but unaware
ComaDiagnosis of Coma
Definition A state of profound unresponsiveness
Clinical features No spontaneous movement
Unresponsive to stimulation by various means
Important causes • Stroke
• Anoxia
• Intoxication-medication and drugs
• Head injury
Diagnostic tests • Lab-drug screen blood levels of certain prescribed
medication electrolytes
• Imaging CT or MRI
April 2007
Coma
April 2007
Vegetative State
April 2007
Vegetative State Jennett & Plum, Lancet 1972
April 2007
April 2007Lancet 2006; 367: 1181–92
April 2007
Minimally Conscious State
April 2007
Locked-in State
April 2007
Lancet 2006; 367: 1181–92
April 2007
Laureys et al. Lancet Neurol 2004; 3: 537–46
April 2007
Laureys et al. Lancet Neurol 2004; 3: 537–46
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