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