What is Coma ?

 A coma, sometimes also called persistent vegetative state, is a profound or deep

state of unconsciousness, persistent vegetative state is not brain-death.
 An individual in a state of coma is alive but unable to move or respond to his or
her environment.
 Individuals in such a state have lost their thinking abilities and awareness of their
surroundings, but retain non-cognitive function and normal sleep patterns. Even
though those in a persistent vegetative state lose their higher brain functions, other
key functions such as breathing and circulation remain relatively intact.
Spontaneous movements may occur, and the eyes may open in response to
external stimuli. Individuals may even occasionally grimace, cry, or laugh.
Although individuals in a persistent vegetative state may appear somewhat
normal, they do not speak and they are unable to respond to commands.

Causes of coma :-

1. Trauma

a. The skull is a rigid box that protects the brain. Unfortunately, if the brain is injured and
begins to swell (edema), there is no room for the additional fluid. This causes the brain to
push up against the sides of the skull and it then compresses. Unless the pressure is
relieved, the brain will continue to swell until it pushes down onto the brain steam, which
then damages the RAS, which subsequently affects blood pressure and breathing control
centers.
b. Coma may occur even with a normal CT scan in this situation. Similarly, head trauma
may cause swelling of the brain without any bleeding, and coma may be the result.
c. Head trauma can cause different types of brain injury. The injury can occur to the brain
tissue itself or may cause bleeding to occur between the brain and the skull.

2. Bleeding (Hemorrhage)

{Intracerebral hemorrhage (intra= within + cerebral=brain + hemorrhage=bleeding) may be

small, but it is associated swelling that may cause damage. Epidural, subdural, and subarachnoid
hemorrhages}

a. The lining of the brain has multiple layers, and these layers can act as potential spaces
where bleeding can occur. Epidural (epi= outside the dura= an outer layer of brain lining)
and subdural (sub=below the dura) may not cause coma immediately, but as the bleeding
continues, it compresses the injured side of the brain and shifts it to the unaffected side.
 Now both cerebral hemispheres are affected and loss of consciousness or coma may
occur; the more swelling, the deeper the coma.
b. Bleeding can occur within the skull or brain without trauma. Blood accumulating in areas
it should not be result with the same problem. Some medical causes include:

• Hypertension (high blood pressure): when blood pressure is too high, and not controlled,
blood vessels in the brain may not be able to tolerate the high pressure and may leak
blood.

• Cerebral aneurysm, or an area in a blood vessel that is congenitally weak and ruptures.
Some people are born with blood vessels that have a weak wall and it gradually balloons,
like a weak spot in an inner tube. At some time in their life, or perhaps never, the weak
spot gives way and blood is spilled into the brain.

• Arteriovenous malformations (AVMs) are abnormal blood vessels where arteries connect
to veins and cause potential weak spots that can leak blood. Normally, arteries branch
into smaller and smaller vessels until they form the smallest set of vessels called
capillaries. Capillaries form meshes where chemicals, nutrients, oxygen and carbon
dioxide are exchanged from the blood stream to individual cells. The capillaries then
merge to form larger blood vessels, the veins. In AVMs, this relationship of artery to
capillary to vein is abnormal.

• Tumors, either benign or malignant, can be very vascular (composed of many veins and
capillaries) and have significant bleeding potential.

3. Swelling

a. While trauma can make the brain swell, other types of injury or insult can cause cerebral
edema (cerebral=brain + edema=swelling due to increased fluid).
b. Whether the insult is lack of oxygen, abnormal electrolytes, or hormones, it may
ultimately result in edema of the brain tissue. As with bleeding, the skull limits the space
available for brain swelling to occur; thus the brain tissue is damaged and its function
decreases the more it is compressed against the bones of the skull.

4. Lack of oxygen

a. The brain requires oxygen to function; and without it the brain shuts down. There is a
very short time to get oxygen back to brain tissue before there is permanent damage.
Most research suggests that the time window is four to six minutes.
b. The body provides oxygen to the brain through the lungs. The lungs extract oxygen from
the air, hemoglobin in red blood cells pick up the oxygen, and the heart pumps blood
through normal blood vessels to cells in the body. If any part of the system fails, the
oxygen supply to the brain can be interrupted.
 c. The most common failure occurs with heart rhythm disturbances. The coordinated
electrical beat of the heart is lost and the heart muscle doesn't squeeze blood adequately;
no blood is pumped to the brain and it stops functioning almost immediately.
d. Lungs can also fail; examples include pneumonia, emphysema, or asthma. In each case,
inflammation in the lung tubes (bronchi or bronchioles) or lung tissue makes it difficult
for oxygen to get into the lungs and transferred into the blood stream.
e. Hemoglobin, a molecule in the red blood cell, attaches oxygen from the lungs and
delivers it to cells for use in metabolism. Anemia, or low red blood cell count, can cause
the brain to fail directly, or more likely it causes other organs like the heart to fail. The
heart, like any other muscle requires oxygen to function. Anemia can occur chronically or
it can be due to an acute blood loss (examples include trauma, bleeding from the
stomach). If the blood loss is slow, the body is better able to adapt and tolerate low
hemoglobin levels; if the bleeding occurs quickly, the body may be unable to
compensate, the result being inadequate oxygen supply to tissues such as the brain.

5. Hypoglycemic coma

a. All cells in the body need glucose and oxygen to perform their functions by aerobic
metabolism (aerobic= with oxygen). While other parts of the body can continue for short
periods of time anaerobically (an=without + aerobic+oxygen), the brain cannot. Without
glucose, the brain stops.
b. Hypoglycemia (hypo=low + glyc=glucose + emia= blood) most often occurs in people
with diabetes who have given themselves too much insulin or have not taken in enough
food.Monitoring blood sugars is critical to avoid hypoglycemic coma.

6. Poisons

a. There are two sources of poisons that can affect the brain, those that we take in (through
ingestion or inhaling) and those that the body generates and cannot dispose of in some
way.
b. If the body can be considered a factory, it needs to have the ability to get rid of the waste
products that are made when the body generates energy. These waste products can cause
different organs in the body to fail, including the brain.
c. The liver performs many functions including glucose and protein manufacturing. It also
breaks down and metabolizes chemicals in the body. When the liver fails different
chemicals like ammonia can accumulate and can cause brain cells to stop functioning.
Hepatic encephalopathy or hepatic coma occurs when the liver fails because of an acute
or chronic injury. The most common is cirrhosis due to alcoholism.
d. The kidneys filter blood to rid the body of waste products. When the kidneys fail, a
variety of waste products can accumulate in the bloodstream and cause direct or indirect
damage to the brain. An example of indirect causes would be an elevated potassium level
 affecting heart electrical activity. Direct causes include uremia, where blood urea levels
rise and are directly toxic to brain cells. Common causes of kidney failure include poorly
controlled diabetes and high blood pressure.
e. The thyroid acts as the thermostat for the body and regulates the speed at which the body
functions. If thyroid levels drop too low, gradually, over a period of time myxedema coma
can occur because of profound hypothyroidism.
f. Ingestions can cause the brain to slow down, speed up or alter its perception of the world.
Some ingestions may cause coma in an indirect way. Acetaminophen is a prime example,
an overdose may cause the liver to fail and few days later subsequent hepatic coma
occurs.
g. Alcohol is probably the most common cause of ingested poison or toxin, leading to
altered mental status and coma. In acute alcohol intoxication, the brain is directly
poisoned. Blood alcohol levels fall when metabolized by the liver, but depth of
intoxication can be so great it shuts off many of the involuntary brain activities that
control breathing and maintain muscle function. Opiates like pain pills or heroin can
cause similar slowing of brain function.
h. Cocaine and amphetamines are the common "uppers" or brain stimulants. These brain
stimulants cause an adrenaline-like body response, thus blood pressure and heart rate
spiral out of control and the risk of heart attack, heart rhythm disturbances, or bleeding in
the brain occur.

Assessment of comatose patients :-

When a patient presents in coma, diagnosis and treatment begin simultaneously. Initial treatment
is aimed at addressing immediate life-threatening issues:

• Are the ABCs intact? Is the patient's airway open? Are they breathing? Do they have
good circulation (a heart beat and blood pressure)?

• Is the patient hypoglycemic? The blood sugar is checked by a quick fingerstick bedside
test and if it is low, glucose is administered.

• Did the patient ingest a narcotic? Naloxone (Narcan) may be given intravenously to
reverse an overdose situation.

a. History remains the important key to the diagnosis. Since the patient cannot be the source
of information, questions are asked of family, friends, bystanders, and rescue personnel.
For example, a person sitting at a bar fell down, hit his head and is in coma. While it
might be easy to jump to the conclusion that he was intoxicated, fell, and bled in his
brain, other scenarios need to be considered. Did he have a heart attack, did he suffer a
stroke, or was this a diabetic medication reaction and the blood sugar is low.
 b. Once the patient has been stabilized with acceptable vital signs, physical examination
will include a complete neurologic assessment. From head to toe, this may include
examination of the eyes, pupils, face movements to assess cranial nerves including facial
movement and gag reflex, extremity movement and reaction to stimulation, tendon
reflexes and other testing of spinal cord function. There is special attention paid to
symmetry in the neurology exam, since lack of movement or response on one side of the
body may be caused by bleeding inside the skull or by stroke. General examination
surveys the skin for cuts, scrapes, wounds, etc.

c. The GCS score will be documented; the deeper the coma, the lower the score.

1. Patient’s most significant person:

 Name: Relationship:

2. Patient's significant friends and family/and relationship:

 Name: Relationship:

3. Patient's favorite hobbies, sports, or interests:

4.Patient's favorite song or type of music:

5. Patient's favorite food, including desserts:

6. Patient's favorite perfume/cologne:

7. Patient's favorite material or texture:

8. Patient's favorite Television program and radio station:

9. Patient's typical daily routine:

 1. Gets out of bed:

 2. Showers:
 3. Goes to work or school:
 4. Relaxes or recreation time:
 5. Goes to bed:

10. Any sensory deficits the patient had prior to injury:

11. Any comments:

Purpose of coma stimulation:-

Coma recovery programs aim to provide multiple sensory stimulation to patients in coma or
vegetative state. It is hoped that with intense and repetitive stimulation, the patient will awaken
and return to a higher level of functioning. Coma arousal therapy is believed to provide the
sensory stimulation needed to activate the reticular system, which is responsible for maintaining
consciousness. These procedures are appropriate for any individual who is in coma or vegetative
state and is medically stable.

Rationale & goals of coma stimulation :-

i. May affect RAS n increase arousal n attention to level necessary to perceive incoming
stimuli
ii. May improve quantity n quality of responses toward purposeful activity
iii. May prevent environmental (sensory) deprivation, which has been shown to retard
recovery and the development of CNS function and further depress impaired brain
functioning
iv. Allows for frequent monitoring of pt's responsiveness
v. May provide opportunities for pt. to respond to environment in an adaptive way
vi. May heighten pts' responses to sensory stimuli and eventually channel them into
meaningful activity

Principles of coma stimulation :-

i. Do no harm
ii. Avoid or minimize stimulation programs with comatose patients that have a
ventriculostomy when ICP and/or CPP are still issues
iii. Control the environment
iv. Organize the stimuli
v. Explain to pt. before and while the stimuli are presentedAllow extra time for pt. to
respond
vi. Conduct sessions frequently
vii. Select meaningful stimuli
viii. Verbally reinforce responses
ix. Try stimulating all the senses
x. Direct treatment toward increasing the frequency and rate of response
xi. Avoid over stimulation
xii. Include participation by family and significant others
Techniques of coma stimulation :-

1. Approaching the Patient

o Identify yourself
o Talk to the patient slowly, and in a normal tone of voice
o Keep sentences short and give the patient extra time to think about what you've
said
o Orient patient to the date, time, place, and reason for being in the hospital, and
explain to the patient what you are going to do

2. Visual Stimulation

o Provide a visually stimulating environment at the bedside, such as colorful,

familiar objects, family photographs (labeled), and TV 10-15 minutes at a time
o Provide normal visual orientation, by positioning patient upright in bed, in the
wheelchair, etc. This also helps decrease complications of prolonged bedrest, such
as pressure sores, breathing problems, osteoporosis, and muscle contractures
o Eliminate distraction to allow patient to focus on visual stimuli, such as a familiar
face, object, photos, and on a mirror
o Attempt visual tracking after focusing is established, i.e. getting the patient to
follow a stimulus with his/her eyes at it moves. Tracking usually begins in the
center or midline.

3. Auditory Stimulation

o Provide regular auditory stimulation at the patient's bedside. All hospital staff
should be encouraged to speak to the patient as they work in the room or directly
with the patient. An information sheet can be posted in the room with information
about the patient's likes and dislikes
o Permit only one person to speak at a time
o Use radio, TV, tape recording of a familiar voice, etc. for 10-15 minutes at
intervals throughout the day
o Direct work to focusing and localizing sound and look for patient's response when
you change the location of a sound, e.g. call the patient's name, clap you hands,
ring a bell, rattle, whistle, etc. 5-10 seconds at a time
o Avoid stimulation that evokes a startled response. This type of stimulation is
counterproductive.

4. Tactile Stimulation
 Tactile input can be facilitory (encourage a desired response) or inhibitory
(discourage/interfere with a desired response). For example, pain and light touch to the
skin tend to produce an inhibitory response, while maintained touch, pressure to the oral
area, and slow stroking of the spine tend to produce a facilitory response. The face, and
especially the lips and mouth area, are the most sensitive.

o Use a variety of textures, such as personal clothing, blankets, stuffed animals,

lotions, etc.
o Use a variety of temperatures, such as warm and cold cloths or metal spoons
dipped for 30 seconds in hot or cold water
o Vary the degree of pressure - firm pressure is usually less threatening or irritating
to the patient than light touch. Examples include grasping a muscle and
maintaining the pressure for 3 -5 seconds, stretching a tendon and maintaining the
stretch for a few seconds, and rubbing the sternum
o Use unpleasant stimuli, such as a pinprick, with caution. Avoid ice to face or
body, as it may trigger a sympathetic nervous system response, i.e. increased
blood pressure, heart rate, and salivation and decreased gastrointestinal activity

5. Movement Stimulation

o Use range of motion exercises, changes in body position such as a single or

repetitive roll, a tilt table to bring the patient to a more upright position, and
movement activities on a therapy mat
o Watch for early physical protective reactions or delayed balance reactions during
these activities

6. Kinaesthetic Stimulation

Slow changes in position tend to be inhibitory, while faster movement patterns tend to
facilitate arousal

o Monitor the patient's blood pressure (and ICP if appropriate) during this
stimulation
o Use position changes that are meaningful and familiar, such as rolling, rocking in
a chair or on a mat, and moving from lying down to sitting
o Avoid spinning, which may trigger seizures, and mechanical input, such as raising
and lowering the hospital bed, which has little functional meaning and produces
limited response

7. Olfactory Stimulation
 o Use after shave, cologne, perfume, favored extracts, coffee grinds, shampoo, and
favorite foods
o Provide the stimuli for no more than 10 seconds
o Avoid touching the skin with the scent, because patient may accommodate the
scent and be less responsive to it
o Use garlic and mustard as noxious stimuli
o Avoid vinegar and ammonia because they irritate the trigeminal nerve

However, there may not be a response to smell stimulation because:

o The olfactory nerve is the most commonly injured cranial nerve in TBI
o Many TBI patients have tracheostomies, which eliminate the exchange of air
through the nostrils and therefore inhibit the sense of smell
o Patients have nasogastric tubes in place, which block one nostril and therefore
decrease the sense of smell

8. Gustatory Stimulation

o Provide taste stimulation, unless patient is prone to aspiration - Use a cotton swab
dipped in a sweet, salty, or sour solution, but avoid sweet tastes if the patient has
difficulty managing oral secretions since sweet tastes increase salivation
o Provide oral stimulation during routine mouth care, unless patient demonstrates a
bite reflex
 Use a sponge-tipped or glycerin swab or a soft toothbrush to diminish
hypersensitivity and abnormal oral/facial reflexes
 Use a flavored cleansing agent, such as mint or lemon, to increase oral
stimulation during routine mouth care.
o Provide stimulation to the lips and area around the mouth. If patient demonstrates
defensiveness to touch, such as pursing lips, closing mouth, or pulling away from
the stimulus, gently continue with stimulation techniques to decrease defensive
reactions and increase level of awareness. Do not attempt feeding of patients in
coma.

Patterns of arousal :-

• Persistent Vegetative State (PVS - in coma 3-6 months after trauma)

o A syndrome of wakeful unresponsiveness in which patients are neither conscious
or in a coma.
o Neocortical damage prevents conscious thought, but the brainstem continues the
motor functions, such as breathing, sleep-wake cycles, coughing, etc.
 o There is no cerebral cortical function (purposeful responding, following
commands, or speaking), but the patient can respond at a subcortical level (i.e.
eye opening, visual tracking, postural reflexes, grasp reflex, etc.)

These patients may be admitted to a rehab program for a trial period of therapy and to
properly evaluate positioning and equipment needs, such as a bed, wheelchair, etc.

• Early Stages of Recovery

o Often characterized by inconsistency of response to stimulation, which may be
affected by time of day, position, and type of input.
o Chart and post the patient's responses, so family and rehab team members can
document the type of stimulus, patient response, and time of day to determine
patterns that indicate increased levels of arousal throughout the day
o Capitalize on the documented periods of alertness and provide meaningful input
in the hope of expanding this state.
• Level III of RLAS - Localized Response
o Increase the frequency, variety, consistency, and rate of response with the goal of
expanding the patient's response and channeling responses into simple activities
o Perform a stimulation oriented program on patients who can attend to an activity,
follow simple verbal or demonstrated commands, and use objects - e.g. catching
or throwing a ball, matching activities, 1-piece puzzles, simple self-care activities.
Progress to a structure oriented program when the patient progresses to Level IV.

Programs :-

• All the senses

• Lasting apprx. 15-20 min
• For 5 times in a day
• Resting period of 2 to 3 hr in between
• Six days a week

Warning signs of sensory overload :-

i. Flushing
ii. Perspiring
iii. Prolonged increase in respiration rate
iv. Agitation
v. Closing of eyes
vi. Sudden decrease in level of arousal
vii. Increase in muscle tone
 Recent advances in coma stimulation therapy :-

 Prolonged coma and vegetative state follow severe TBI in about 1 out of 8 pts with
severe closed-head injury
(Levin 1991)
 The outcome for individuals in coma or vegetative state with non traumatic brain injury is
worse than that for those with TBI
 (Sazbon 1993)
 1950’s: Institute for the Achievement of Human Potential (I.A.H.P.):
 Prog. of environmental sensory input, at frequency, intensity, and duration far greater
than those in usual hospital setting, could enhance speed and degree of recovery from
coma
 “In comatose patients, although problem is primarily cerebral, there is a condition of
environmental deprivation that could lead to widespread impairment of intellectual and
perceptual processes accompanied by changes in cerebral electrical activity”
 (Lewinn 1978)
 The use of sensory stimulation for coma and vegetative state gained popularity in western
world, despite a lack of scientific evidence (Wood 1991, Zasler 1991, Andrews
1996,Giacino 1997)
 “Clinical experience has shown that patients exposed to an undifferentiated bombardment
of sensory information lose ability to process information due to background noise
(habituation)
(Wood 1991)
 ’Sensory Regulation’ approach: based on the concept of regulating the way in which
stimulations are delivered (i.e. create a quiet environment regulate the way in which staff
communicate with pt,etc.)
o (Wood 1992)

I. Autonomic reactivity to sensory stimulation is related to consciousness level after severe

traumatic brain injury

(Clinical Neurophysiology 117 (2006)1794–1807)

Results:

 Both (HRV) and skin conductance level (SCL) in reaction to sensory stimulation changed
with recovery to consciousness.
  Indices of HRV and SCL that represent sympathetic activity of the autonomic nervous
system (ANS) increased with recovery, whereas indices that represent parasympathetic
activity decreased.

Conclusions:

 Recovery to consciousness is related to changes in SCL and HRV during sensory

stimulation.
 ANS reactivity to environmental stimulation can give objective information about clinical
state of TBI pts, and can contribute to decision-making in treatment policy of unresponsive
patients.

Significance:

 Autonomic reactivity can be informative concerning how a severely damaged nervous

system reacts to environmental stimulation and how, in a recovering nervous system, this
reactivity changes.

II The influence of acoustic and tactile stimulation on vegetative parameters and EEG in
persistent vegetative state

(Ingo Keller, Angelika Hülsdunk, Friedemann Müller)

Conclusion:

 Non-specific acoustic stimulation and tactile stimulation led to a significant increase in

skin conductance response and in EMG activity
 Greatest responses were obtained in tactile stimulation condition, which also showed an
effect on heart rate and EEG activity
 It could not be concluded that hearing the voice of relatives has an impact on information
processing in vegetative state.
 Pharmacological stimulation raises baseline activity of reticular activating system but
shows no interaction with sensory stimulation.

III. Sensory stimulation for brain injured individuals in coma or vegetative state (Review)

(Lombardi F, Taricco M, De Tanti A, Telaro E, Liberati A)

Types of intervention Comparison of:-

i. ’Intense Multisensory Stimulation Programmes’ (IMS)

ii. Formalized Not-Intensive Stimulation Programmes’
iii. Sensory Regulation Programmes’

V/S

i. Standard rehab. Treatment

1. Intense Multisensory Stimulation Programmes’ (IMS) –

e.g. Doman’s programme: stimulatory cycles lasting approx 15 - 20 minutes, repeated every hour
for 12-14 hours per day, six days a week.

2. Formalized Not-Intensive Stimulation Prog. –

e.g. Mitchell and Wilson’s prog.: cycles of stimulation 10-60 minutes twice a day

3. Sensory Regulation Prog. –

e.g. Wood prog. : single brief sessions of stimulation in a quiet environment completely free of
noise

4. Standard Rehab. Treatment:

Aimed at reducing behavioural,cognitive and motor complications, with usual nursing

interventions, swallowing treatment, nutrition, hydration, physical therapy, and neuro-
pharmachological interventions.

Types of outcome measures:-

i. Duration of unconsciousness (including coma and vegetative state): time between trauma
and objective recovery
ii. of the ability to respond to verbal commands.
iii. Level of consciousness, as measured by GCS
iv. Level of Cognitive Functioning (LCF) (Hagen 1979)
v. Functional outcomes, as measured by Glasgow Outcome Scale (GOS) (Jennett 1975) or
by Disability Rating Scale (Rappaport 1982)
vi. Adverse effects i.e. increased ICP
A. Study 1: Johnson 1993

• Methods: RCT
• Randomization method: not specified
• Participants 14 male adults, affected by TBI from road traffic accident, with GCS < = 8,
consecutively admitted within 24 hours to the intensive care unit.
• Experimental group: 7 subjects, mean age 27.7 (12.3), mean GCS: 4.8 (1.9)
• Control group : 7 subjects, mean age 31.4 (11.2) mean GCS: 4.8 (1.4)
• Pts with neurological or psychiatric disorders, alcohol or drug abuse, or previous head
injuries were excluded.
• Interventions Experimental group: stimulation of five senses for 20-minute a day for all
their stay in ICU (median stay 8.1 days)
• Order of stimulus presentation was randomized
• Control group were not stimulated during same period (stay medium 3.7 days).

OUTCOMES

i. GCS
ii. State of ventilation
iii. Spontaneous eye movts.
iv. Oculocephalic response
v. Oculovestibular response
vi. Assessed daily Catecholamine levels, Serotonin level, Acetylcholinesterase level, 3-
methoxy,4-hydroxyphenylglicol, skin conductance
vii. heart rate, assessed 20 minutes pre- and post-treatment period.

B. Study 2: Kater 1989

• Methods: Controlled clinical trial. 2 gps. matched for age, sex and type of injury
• Participants 30 pts with traumatic brain injury (mean age 28 y, range 18-47, 18 male and
12 female), at least 2 weeks from the trauma, admitted at 2 different health care facilities
• GCS :3-14
• length of coma: 6 hrs - 6 months
• Subjects in control group (15) matched with pts in experimental gp (15) on basis of age,
sex, type of injury, GCS and length of time post-injury.
 • Interventions Experimental group: stimulation of 6 modalities: visual, auditory, olfactory,
cutaneous, kinesthetic, oral
• Treatment: started 2 weeks from trauma, 45 min., twice a day, 6 days/week for 1 to 3
month period
• Relatives encouraged to apply sensory stimulation.
• Control group received nursing care without planned, structured sensory stimulation

OUTCOMES

i. Level of Cognitive Functioning (LCF) measured 2 weeks post injury (baseline) and at 3 months
post injury
ii. Inclusion criteria were broad (e.g. GCS from 3 to 14)

C. Study 3: Mitchell 1990

• Methods: Controlled clinical trial. Two groups matched on demographic characteristics,

type and location of head injury, surgical intervention and GCS on admission to hospital
• Participants: 24 patients with traumatic brain injury divided in 2 groups of 12 patients,
treated in the same Neurological Unit.
• Treatment group: 10 male and 2 female, mean age 22.3 (6.15), range 17-40; range GCS
admission 4-6
• Control group : 10 male and 12 female, mean age 22.75 (6.77), range 17-42; range GCS
admission 4-6
• Interventions Experimental group: visual, auditory, olfactory, tactile, gustatory,
kinesthetic and vestibular stimulation
• The stimulation sessions started from 4 to 12 days following injury (mean 7.08 days).
Treatment lasted 1 hour for 1 or 2 times a day
• Control group did not receive arousal procedure at any time while in coma.

OUTCOMES

i. Total duration of coma (days)

ii. Glasgow Coma Scale (GCS)

Main results:-

 3 studies identified with 68 pts in total

 Overall methodological quality was poor and studies differed widely in terms of
outcomes measures, study design and conduct.
 Did not carry out any quantitative synthesis but reviewed results of available studies
qualitatively.
Author’s conclusions:-

I. There is no reliable evidence to support, or rule out, the effectiveness of multi sensory
programmes in patients in coma or vegetative state.
II. The review found there is no strong evidence to determine whether sensory stimulation
benefits people in coma
 Assignment on

COMA
STIMULATION
THERAPY

Submitted by – Submitted to-

Darshika Vyas Dr. Sharmishtha Gadgil

(MPT II year)