ALTERED STATES OF CONCIOUSNESS

Hendro BIrowo

CONSCIOUSNESS

Consciousness is the state of awareness of the self and environment Awareness of internal or external world

Component of conciousness

AROUSAL

Reticular system + projections to thalamus

CONSCIOUSNESS
thalamus, cerebral cortex, and their white matter connections + functioning reticular system

AWARENESS

Conciousness has two mayor components

Content
is represent of sum the all functions mediated of cerebral cortical level, including both a cognitive and affective response if a reduced of conc. Is not due to focal impairment to cognitive function, but the rather to a global reduction in the level of behavioral responsiveness of conc.

Arousal

Anatomy of consciousness
Arousal
requires both the reticular formation and the cerebral hemisphere. The reticular component for arousal reside in rostral midpons, midbrain (mesencephalon) and thalamus to cortex cerebri. These they termed as the ascending reticular activating system (ARAS).

Content of consciousness
is on cerebral cortex.

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 LC 2.Serotonin from the dorsal and me dian RN 3.DA from ventral periacque. Gray matter 4.His from TMN 5.ORX and MCH from Lat Hypothal 6.Ach and GABA from the Basal Fo rebrain

Disorders of Consciousness
Disorders of consciousness include:
Disorders in which the Level of consciousness is impaired; e.g. acute confusional state, coma Disorders in which the level of consciousness is normal, but the Content is altered; e.g. dementia or amnistic disorders

Disorders of Consciousness
Level of consciousness

Characterized by impaired arousal or wakefulness Result from acute lesions of the: Ascending Reticular Activating System Both Cerebral Hemispheres
Content of consciousness Cognitive function

Disorders Affecting the Level of Consciousness

Coma Most severe degree Pt cannot be aroused Acute Confusional State or Delirium Less severe degree Can present as an acute or subacute condition Pt is drowsy & disoriented, but responds to stimuli

Disorders of Consciousness

Disorders Affecting the Content of Consciousness

Can be altered w/o affecting the Level of consciousness Examples: Dementia Widespread deterioration of mental function Results from diffuse & chronic pathological process

Qualitative level of conciousness

Normal waking state ( compos mentis)

Somnolence
Sopor (Stupor)

coma

Quantitative level of conc. Glasgow Coma Scale (GCS)

Estimate :
Eye response ( E )
Motor response ( M ) Verbal response ( V )

GCS
13 15 mild 9 12 moderate

3 - 8 severe

Eye response
Eyes open spontaneously Eye opening to verbal command Eye opening to pain No eye open =4 =3 =2 =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).

1.Diffuse and multifocal processes. Metabolik : hypo or for example hyperglicemia, hepatic failure, renal failure, toxin induced (drugs,alcohol), infectious, 2 Supratentorial lesions: Haemorrhage : extradural(epidural),subdural, intracerebral. Infarction : embolic, thrombotic. Tumours : primary, secondary, abscess. 3. Infratentorial lesions. Haemorrhage Infarction Tumours Abscess : cerebellar, pontine. : brainstem. : cerebellum. : cerebellum.

Differential Diagnosis of Coma

Disorder
Stroke

Distinguishing clinical feature

Acute onset Neurological deficit

Making the diagnosis

Clinical diagnosis of coma and sign of severe brain damage in focal distribution approriate to the coma Imaging : infarct or haemorrhage History of cardiac arrest or other cause of anoxia Clinical feature of coma with or without myoclonus Clinical feature are nonspecific. Suspicion is key Drug screen is critical

Anoxia

Coma following episode of anoxia Myoclonus and/or seizure are often seen Multifocal sign with unequal region of anoxic Coma with lost of brainstem reflexes without other focal sign History of substance ingestion

Intoxication

Differential Diagnosis of Coma

Disorder
Head injury

Distinguishing clinical feature

Coma following head injury with or without focal sign Mental status fluctuate with cerebral edema and other factor Overts sign of injury are present

Making the diagnosis

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
Patient imobile, on casual observation appear to be comatose Patient retain vertical eye movement and communication is possible with this condition

Lab results show abnormality : electrolytes, etc. Imaging and lab result do not show other cause consider another causes
Able to communicate with eye movement Brainstem infarction may see in MRI or CT

Locked in syndrome in brainstem infarction

Differential Diagnosis of Coma

Disorder
Pseudocoma

Distinguishing clinical feature

Clinical appearance of coma with preservation of brain function Patient may be unaware of the pseudocoma or be intentionally unresponsiveness

Making the diagnosis

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

Cheyne stokes respiration

This respiration pattern is associated with periods hyperpnoe alternating with period apnoe, usually from 10-20 seconds. Bilateral cerebral hemisphere dysfunction (diencephalic level).

Central neurogenic hyperventilation

Appears and its noted dysfunction midbrain or upper pons. Rapid respiration up to 40-50x/mnt PO2 must be greater than 70-80 mmHg. If the PO2 level isnt above the level hipoxemia Cardiac, pulmonary, and metabolic problem must be ruled out as possible causes of the hiperventilation.

Apneustic respiration noted in lower pontine lesions,consist of prolong inspiratory phase with a pause at full inspiration.

Cluster breathing
also signifying lower pontine damage, is characterized for by disorderly sequence of closely grouped respirations followed by apnoe

Ataxic respirations

signify a lower pontine or medullary respiratory center problem. The pattern is chaotic and haphazard with irregular pauses its lead to gasping and eventual cessation of breathing.

Apnea
Occurs when lesions encroach on the ventral respiratory group in the ventrolateral medulla bilaterally

Pupil (size in mm) in ambient light, and in reaction to direct/consensual light.

1. Equal and reactive pupils Toxic/metabolic cause
2. Unequal.

Fixed and dilated pupil three oculomotor palsy. Herniation : if larger pupil associated with ipsilateral 3rd nerve extra ocular muscle palsy. Possible horner syndrome,consider carotid occlusion/dissection.
3. Bilateral pupil abnormalities. Pinpoint- pontine lesion Bilateral fixed and dilated(7-10 mm): sub total damage to medulla or immediate post anoxia or hypothermia. Midposition ( 4 6 mm ) and fixed: more extensive md brain lesion.

Pupillary Responses in Various Lesions

Signs of increased ICP/Herniation

Pupils
Unilateral dilated pupil Bilateral small poorly reactive pupils Third nerve palsy Sixth nerve palsy Can be assessed by cold caloric Signs of papilledema?

Eye movements

Fundoscopy

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 :
edema.

Cerebral contusions, hematomas, abscesses, neoplasms, cerebral

 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.

 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
April 2007

Coma
Diagnosis of Coma

Definition Clinical features

Important causes

A state of profound unresponsiveness No spontaneous movement Unresponsive to stimulation by various means

Stroke Anoxia Intoxication-medication and drugs Head injury Lab-drug screen blood levels of certain prescribed medication electrolytes Imaging CT or MRI

Diagnostic tests

Coma
state of unresponsiveness in which patient lies with eyes closed, cannot be aroused, and has no awareness of self and surroundings

stimulation cannot produce spontaneous periods of wakefulness and eye-opening in patients in a coma, unlike patients in a vegetative state
In general, comatose patients who survive begin to awaken and recover gradually within 24 weeks can result from:
diffuse bihemispheric cortical or white-matter damage or focal brainstem lesions that affect the pontomesencephalic tegmentum or paramedian thalami bilaterally
April 2007

Vegetative State
vegetate = live merely a physical life devoid of intellectual activity or social intercourse awake but unaware of themselves or environment necessary conditions for diagnosis:
no response to visual, auditory, tactile or noxious stimuli of a kind suggesting volition or conscious purpose no evidence of language comprehension or meaningful expression brainstem is mostly spared whereas the grey and white matter of both cerebral hemispheres are widely and severely damaged
April 2007

Vegetative State
Persistent vegetative state

Jennett & Plum, Lancet 1972

vegetative state remaining 1 month after acute traumatic or non traumatic brain damage Permanent vegetative state irreversible regarded as permanent 3 months after non-traumatic brain damage or 12 months after traumatic injury

April 2007

April 2007

Lancet 2006; 367: 118192

April 2007

Minimally Conscious State

not in a vegetative state but are unable to communicate consistently show limited but clear evidence of awareness of themself or their environment, on a reproducible or sustained basis, by at least one of the following behaviours:
following simple commands gestural or verbal yes/no response (regardless of accuracy), intelligible speech purposeful behaviour

Further improvement is more likely than in patients in a vegetative state.

April 2007

Locked-in

State

quadriplegia and anarthria resulting from the disruption of corticospinal and corticobulbar pathways
sustained eye opening (bilateral ptosis should be ruled out as a complicating factor) awareness of the environment aphonia or hypophonia quadriplegia or quadriparesis vertical or lateral eye movement or blinking of the upper eyelid to signal yes/no responses

Eye or eyelid movements are main method of communication

Structural brain imaging with MRI may show isolated lesions (bilateral infarction, haemorrhage, or tumour) of the ventral portion of the basis pontis or midbrain.

April 2007

Lancet 2006; 367: 118192

April 2007

Laureys et al. Lancet Neurol 2004; 3: 53746

April 2007

Laureys et al. Lancet Neurol 2004; 3: 53746

April 2007