1. Apakah pasien syncope, kejang apakah brainstemnya terganggu?

Apakah kondisi lain yang menyebabkan

kehilangan kesadaran?
Apakah Pasien syncope, kejang?
Syncope = a transient, self-limited loss of consciousness due to acute global impairment of cerebral blood
flow.
Seizure =
Brain stem pasti terganggu

What are the causes of coma or unconscious?

UNCONSCIOUS
As follows (remember the mnemonic AEIOU–DAMH):
• Apoplexy: Cerebral haemorrhage, subarachnoid haemorrhage etc.
• Epilepsy.
• Infection (e.g., encephalitis, meningitis, cerebral malaria, severe septicaemia).
• Opium poisoning.
• Uraemia (renal failure).
• Diabetes mellitus (ketoacidosis, hypoglycaemia, lactic acidosis, hyperosmolar nonketotic diabetic coma or
hyperglycaemic hyperosmolar state).
• Drug poisoning such as sedative.
• Alcohol.
• Metabolic: Metabolic acidosis.
• Hypoglycaemia, hypoxaemia, hypertensive encephalopathy, hepatic coma, hypothyroidism (myxoedema
coma), hyponatraemia, hypothermia, hyperpyrexia, head injur

2.Mekanisme penurunan kesadaran ( syncope, coma dll)

Physiology kesadaran
[https://med.unhas.ac.id/kedokteran/wp-content/uploads/2016/09/Bahan-Ajar-Kesadaran-Menurun.pdf]
● There is a constant interaction between the cerebral hemisphere and the reticular formation in the brain
stem.
● Awareness can be described as a state of constant vigilance to the state of the environment or the
sequence of our thoughts. This means that a person is aware of all intake from the five senses and is
able to react optimal for all stimuli both from outside and from within the body
● In normal human awareness, it can be anticipated and that the reaction can be returned to full
awareness again. To be honest, it's a complicated interaction between the reticular formation, the
cerebral cortex and the brain stem
● During the human sleep, at the part of the brain of the rostral area, called the arousal center, an
activity center that eliminates synchronization (doing desynchronization), in which the sleep state is
changed to an alert alert state
● When the sleep state is not activated, then the nucleus inhibition and mesencephalic, which allows the
reticularis on the upper part of the pons to be activated
● This in turn stimulates the cerebral cortex and the peripheral nervous system, both of which then sends
many positive feedback signals back to the reticular nuclei to keep the system active. As soon as the
 alert state arises, then there is a natural tendency to maintain this condition, as a result of all the
positive feedback activity.
● The input mechanism has an improvement mechanism.
● Specific afferent impulses are typical afferent impulses that include protopathic, proprioceptive and
impulses the five senses. The conduction of these impulses from receptor points on the body by
pathways spinothalamic, medial lemniscus, geniculo-calcarine pathways and so on to the point in the
primary perceptive cortex. These specific afferent impulses that reach the cortex will produce
awareness that is specific in nature, namely the feeling of pain in the legs or feet other places, sight,
smell or hearing.
● These specific afferent impulses through their collateral branches will become non-specific impulse
because of its transmission through non-specific afferent pathways consisting of neurons in the
reticular substance of the spinal cord and brainstem to the nucleus thalamic intralaminar
neurons (and are called alertness-inducing neurons) take place multi synaptically, unilaterally and
laterally, and stimulates the nucleus emits impulses that activate the entire cortex diffusely and
bilaterally known as the diffuse ascending reticular system.
● Neurons throughout the cerebral cortex stimulated by these non-specific afferent impulses are called
neuron vigilance bearers. These non-specific afferent pathways carry impulses from any point on the
body to points on all sides of the cerebral cortex. So in fact, it is the lower centers of the brain, the
reticular substance which contains diffuse non-specific pathways, which give rise to
“awareness” in the cortex cerebral.
● The degree of consciousness itself is determined by the number of driving neurons or active
alert-carrying neurons. The main functional elements of neurons is the ability to be stimulated to give
rise to an action potential. It is also supported by processes that maintain the life of neurons as well as
cellular elements of the brain through biochemical processes, because the degree of consciousness
depends on the number of active neurons. There is a good disturbance on alert-carrying or
alert-activating neurons that cause impaired consciousness.

Pathophysiology of unconsciousness
 ● result of various kinds of disorders or diseases, each of which in the end interfere with the function of
the reticular activating system directly or indirectly
● three types of lesions/mechanisms each of which impairs function reticular activating system, either
directly or indirectly
○ Diffuse brain dysfunction
■ Metabolic or submicroscopic processes that suppress neuronal activity.
■ Lesions caused by metabolic or toxic abnormalities or general electric discharges
(seizures) are thought to be subcellular or molecular, or scattered microscopic lesions.
■ Extensive bilateral cortical and subcortical injury or thalamic damage severe disease
resulting in the interruption of thalamocortical impulses or destruction cortical neurons
may be traumatized (contusions, diffuse axonal injury),stroke (bilateral cerebral
infarction or hemorrhage).
■ A number of diseases have a direct influence on the metabolic activity of neurons in the
cerebral cortex and the central nuclei of the brain such as meningitis, viral encephalitis,
hypoxia or ischemia which may occur in cases of cardiac arrest.
■ In general, losing consciousness in this state is equivalent to decreased cerebral blood
flow or cerebral metabolism
○ Direct effect on brain stem
■ Lesions in the brainstem and lower diencephalon that damage/inhibit reticular activating
system
■ Anatomic lesions or destructive lesions are located in the thalamus or midbrain where
ARAS neurons are directly involved
■ Less common
■ This pathoanatomic pattern is a hallmark of brainstem stroke due to occlusion basilar
artery, thalamic and upper brainstem hemorrhages, and traumatic injury
○ Effects of compression on the brain stem
■ Primary or secondary causes of compression
■ Mass lesions that can be seen easily.
■ Tumor mass, abscess, infarction with massive edema or hemorrhage intracerebral,
subdural and epidural. Usually these lesions only affect part of the cerebral cortex and
white matter and most of the cerebrum remain intact. But these lesions distort deeper
structures and cause coma due to lateral compression of the structure inner middle and
temporal lobe tentorial herniation which results in compression of the mesencephalon
and subthalamic areas of the reticular activating system, or there are more widespread
changes throughout the hemisphere.
■ Cerebellar lesions as a secondary cause can also compress the reticular area of the
upper brainstem and slide it forward and up.
■ In cases of prolonged coma, pathological changes associated with lesions are found all
parts of the nervous system cortex and diencephalon

Based on the anatomy-pathophysiology, coma is divided into:

1) Cortical-bihemispheric coma, i.e. coma that occurs due to -carrying neurons alertness is impaired.
2) Diencephalic coma, divided into supratentorial, infratentorial, combination coma supratentorial and
infratentorial; In this case, alertness-inducing neurons powerless to activate alertness-carrying neurons.

In The experiment there can be cause of coma, if there is decortication or destruction of the thalamic
intralaminar nuclei or if the gray matter around the Sylvius aqueduct. There will be nonspecific ascending
impulse leading to coma.
Coma can also occur if there is a disturbance in either the initiating neurons' alertness and
alertness-carrying neurons that cause these neurons to not function properly and not be able to react to
racing from outside and from within the body itself. There is functional impairment in alertness-carrying
neurons, causing bihemispheric cortical coma, whereas if there is a disturbance in the alertness-promoting
neuron, cause diencephalic, supratentorial or infratentorial coma.

Decreased physiological function in the presence of pathological changes that occurs in prolonged coma is
closely related to systemic lesions diencephalic cortical neurons. These simple process can be leading to
coma from the cause:
destruction both
● morphological (bleeding, metastasis, infiltration),
● biochemical (metabolism, infection) and
● compression of the most rostral brainstem reticular substance (intralaminar nuclei)
● diffuse disturbances in both cerebral hemispheres

Eventually pathological of decrease in consciousness level can be shown in the process:

● excessive sleep (hypersomnia) and other alertness that below the level of consciousness
● Lethargy (, akinetic mutism (a syndrome of variable severity caused by lesions of both
medial frontal lobes causing decreased motivation), stupor (a state of near-unconsciousness or
insensibility) and coma
This is dangerous if the alertness has decreased, in other words, if there is no neuronal transmission between
the brainstem to the cerebrum, then the brain will experience the compression at the junction between the
mesencephalon and the cerebrum. There could be the possibility of developing a pituitary tumor that results in
irreversible coma. When all these signals are lost, the level of activity in the excitatory area will
decrease suddenly and brain activity will immediately decrease greatly, to near a permanent coma

3. Physical examination pada pemeriksaan kehilangan kesadaran? + Pemeriksaan tambahan kesadaran

[https://med.unhas.ac.id/kedokteran/wp-content/uploads/2016/09/Bahan-Ajar-Kesadaran-Menurun.pdf]

Lower limb
Inspection:
• Wasting (mention whether of right, left or both, involving thigh or leg).
• Skin change (shiny, pigmented, rough, ulceration, hair loss, gangrene). See the tip of the toes and soles.
• One leg is smaller than the other (found in old poliomyelitis).
• Pes cavus (involving right or left or both feet).
• Fasciculation (if not visible, tap the muscle with your fingers).
• Swelling of calf muscles (pseudohypertrophy of calf muscles).
• Joint abnormality (deformity or swelling, signs of inflammation).

Palpation:
1. Bulk of the muscles (measure with tape from a particular point):
• Unilateral wasting (in old poliomyelitis).
• Generalized wasting (in MND, polyneuropathy, lower motor neuron lesion).
• Isolated anterior wasting in thigh (in diabetic amyotrophy).
• Wasting in the leg that stops suddenly at a certain level (in Charcot–Marie–Tooth disease).

2. Muscle tone: Tell the patient, ‘Keep your limbs relaxed’. Now the examinee should do the following—
• Lift the leg and allow it to fall.
• Palpate the muscle and perform side to side movement of the limbs.
• Lastly, passive movement of the limb (in irregular fashion—flexion and extension).

3. Test for clonus (ankle and patella). 4. Muscle power (against resistance): If any weakness, mention grading
of weakness. To test, ask the patient to follow your instructions as follows:
• Hip flexion: ‘Raise your leg straight, do not let me push it down’. (Prime mover: iliopsoas—L1 & L2).
• Hip extension: ‘Push your leg down, do not let me pull it up’. (Prime mover: glutei muscles— L4 & L5).
• Hip adduction: ‘Push your thighs inwards, do not let me move them apart’. (Prime movers: adductors of thigh,
such as adductor longus, brevis and magnus—L2, L3 & L4).
• Hip abduction: ‘Push your thigh outwards. Do not let me push them inward’. (Prime movers: gluteus medius
and minimus, sartorius and tensor fasciae latae—L4, L5 & S1).
• Knee flexion: ‘Bend your knees, do not let me straighten them’. (Prime mover: hamstrings such as biceps
femoris, semimembranosus and semitendinosus—L5, S1 & S2).
• Knee extension: ‘Straighten your knees, do not let me stop doing’. (Prime mover: quadriceps femoris—L3 &
L4).
• Plantar flexion of ankle: ‘Push your foot downwards against my hand’. (Prime movers: gastrocnemius,
plantaris and soleus—S1 & S2).
• Dorsiflexion of ankle: ‘Push your foot upwards against my hand’. (Prime movers: tibialis anterior, extensor
digitorum longus and extensor hallucis longus—L4 & L5).
• Inversion of foot: ‘Push your foot inward against my hand’. (Prime movers: tibialis anterior and posterior—L5
& S1).
• Eversion of foot: ‘Push your foot outward against my hand’. (Prime movers: peroneus longus and brevis—L5
& S1).
• Extension of great toe: ‘Push your great toe upwards and do not let me push it down’. (Prime mover: extensor
hallucis longus—L5).

5. Reflexes:
• Knee (L3 and L4).
• Ankle (S1 and S2).
• Plantar (L5, S1 and S2): Tell the patient, ‘I am going to tickle the bottom of your foot, with an orange stick at
the outer portion of the sole’. Mention your finding, ‘Plantar is extensor or flexor or equivocal or cannot be
elicited’.

6. Superficial reflexes:
• Abdominal reflex (T6 to T11): Elicited by lightly stroking the abdominal wall diagonally towards umbilicus in
each of the four quadrants of abdomen. If positive, reflex contraction of abdominal wall occurs. It is absent in
upper motor neuron lesion (early loss is found in multiple sclerosis).
• Cremasteric reflex (L1 & L2): Stroke the inner part of thigh in downward direction. Normally, contraction of
cremasteric muscles pulls up the scrotum and testis on the side stroked.
7. Co-ordination (Explain and show it to the patient.):
• Heel–shin test: ‘Please raise your leg, put your heel upon the knee of other leg and run it along the shin’.
(Repeat the same for other leg).
• Foot taping test: Keep your hand at a little distance from ball of patient’s foot and ask the patient to tap it
rapidly on your hand (dysdiadochokinesis).

8. Sensory test: Explain to the patient with light touch by cotton-wool in normal area such as forehead. Ask the
patient ‘Can you feel it’? Now touch the leg or foot. Ask the patient, ‘Can you feel it’? If no, continue to touch
above, until the patient can feel to find out the level of sensory loss.
• Light touch (cotton-wool).
• Pin prick. Perform the test according to the nerve distribution:
• Outer thigh L2 (upper thigh).
• Inner thigh L3 (also around knee).
• Outer leg L5 (up to medial foot).
• Inner leg L4.
• Medial foot L5.
• Lateral foot S1.
• Vibration sense (with 128 Hz tuning fork): Always explain the patient first by plucking a tuning fork and
placing it over the sternum. Then repeat it without vibration. Now, test is done placing the vibrating fork on
bony prominence such as side of great toe, medial malleolus. If impaired, it may also be tested in knee and
anterior superior iliac spine.
• Position sense (in great toe, always explain this to the patient.)

9. Test for proximal myopathy: ask the patient to stand up from sitting without support. Unable to do in proximal
myopathy.

10. Test for Rombergism: Ask the patient to stand with feet together and close the eyes. In positive case, the
patient tends to sway or fall. Be careful to protect the patient from falling. If positive, indicates sensory ataxia,
dorsal column lesion (e.g., subacute combined degeneration, tabes dorsalis). In cerebellar lesion, positive in
both closed and open eyes.

11. Gait:
• Ask the patient to walk, look any abnormality such as hemiplegic gait, foot drop, scissor gait.
• Look for festinant gait. Also ask to turn quickly (in Parkinsonism, unable to turn quickly).
• Ask the patient to walk heel-to-toe (to exclude midline cerebellar lesion, in which ataxia may be present).
• Ask the patient to walk on toes (S1 lesion will make it impossible).
• Ask the patient to walk on heel (L4 and L5 lesion will make it impossible).

12. Finally, look at the spine to see any deformity, scar, gibbus and local tenderness
Glasgow coma scale

4. Anamnesa pada pasien yang kehilangan kesadaran (sesudah recovery)

Dalam kasus gangguan kesadaran, auto-anamnesis masih dapat dilakukan bila gangguan kesadaran masih
bersifat ”ringan”, pasien masih dapat menjawab pertanyaan (lihat pemeriksaan Glasgow Coma Scale/ GCS).
Hasil auto-anamnesis ini dapat dimanfaatkan untuk menetapkan adanya gangguan kesadaran yang bersifat
psikiatrik – termasuk sindrom otak organik atau gangguan kesadaran yang bersifat neurologik (dinyatakan
secara kualitatif maupun kuantitatif ke dalam GCS). Namun demikian arti klinis dari anamnesis perlu dicari dari
dengan hetero-anamnesis, yaitu anamnesis terhadap pengantar dan atau keluarganya. Berbagai hal yang
perlu ditanyakan pada saat anamnesis adalah sebaai berikut:
i. Penyakit yang pernah diderita sebelum terjadinya gangguan kesadaran, misalnya diabetes melitus,
hipertensi, penyakit ginjal, penyakit hati, epilepsi, adiksi obat tertentu
ii. Keluhan pasien sebelum terjadinya gangguan kesadaran, antara lain nyeri kepala yang mendadak atau
sudah lama, perasaan pusing berputar, mual dan muntah, penglihatan ganda, kejang, kelumpuhan anggota
gerak.
iii. Obat-obat yang diminum secara rutin oleh pasien, misalnya obat penenang, obat tidur, antikoagulansia,
obat antidiabetes (dapat dalam bentuk injeksi), antihipertensi.
iv. Apakah gangguan kesadaran terjadi secara bertahap atau mendadak, apakah disertai gejala lain / ikutan?
v. Apakah ada inkontinensi urin dan / atau alvi?
vi. Apakah dijumpai surat tertentu (misalnya ”perpisahan”)?

WO
1. Jelaskan anatomi central nervous system yang berpengaruh ke kesadaran
● The reticular activating system (RAS) participates in fight-or-flight responses -> or the reticular
formation, that plays plays a central role in the regulation of the state of consciousness and arousal
● The RAS controls waking and sleep, so that sleep patterns will be dysregulated.
● It consists of a complex network of interconnected circuits of neurons in the tegmentum of the brain
stem, the lateral hypothalamic area, and the medial, intralaminar, and reticular nuclei of the thalamus
● Many of these neurons are serotonergic (using serotonin as their neurotransmitter), or noradrenergic.
Axons from these nonspecific thalamic nuclei project to most of the cerebral cortex, where they
modulate the level of activity of large numbers of neurons.

● The term reticular formation, that means from the characteristics appearance of loosely packed cells of
varying sizes and shapes, embedded in a dense meshwork of cell processes, including dendrites and
axons.
● Though the reticular exact position in the anatomical structure is not well defined because this involves
the neurons, that located in the diverse part of the brain
● However, the important function to maintain the arousal and consciousness behaviour
● As well as the ascending projection (to the cortex), there would be descending axon, which then
enters through the spinal cord into the reticulospinal tract.
● Activity in corticospinal axons modulates spinal reflex activity and may also modulate sensory input by
regulating the gain at synapses within the spinal cord. The reticulospinal tract also carries axons that
modulate autonomic activity in the spinal cord.
The function of the arousal and consciousness
1. Arousal
● This is functioned from the reticular formation. As there will be excited from several stimuli,
which can be somatosensory, auditory, visual, and visceral sensory systems, that will be
conducted by the collaterals.
● Then the reticular formation performs the non specific function and increases the alertness.
● The behaviour arousal is independent of the modality of stimulation and is accompanied by
electroencephalographic changes from low-voltage to high-voltage activity over much of the
cortex
● So the flow would be: stimulus -> nonspecific thalamic regions -> cortex (located in teh distal
dendritic part of the large pyramidal cells)
● So if there is a chance that the reticular formation is destroyed or depressed by anesthesia,
sensory stimuli still produce activity in the specific thalamic and cortical sensory areas, but they
do not produce generalized cortical arousal.
2. Consciousness
 ● Many regions in the cerebral cortex generalise the arousal when it is stimulated. Because of the
different attributes of the external world (eg, color, shape, location, sound of various external
stimuli) are represented in different parts of the cortex, it has been suggested that “binding” of
neural activity in these different areas is involved in conscious actions and conscious
recognition.
● Arousal, which is abolished by lesions in the mesencephalic reticular formation, does not
require an intact corpus callosum, and many regions of the cortex can be injured without
impairing consciousness.
● The cortex and the mesencephalic reticular activating system are mutually sustaining areas
involved in maintaining consciousness. Lesions that destroy a large area of the cortex, a small
area of the midbrain, or both produce coma

Coma Syncope

Onset sudden Profound

Duration Brief Prolong

Intracranial causes Extracranial causes

(include head injuries,
cerebrovascular
accidents, central
nervous system
infections, tumors, and
increased intracranial
pressure)
●vascular disorders
(shock or hypotension
caused by severe
hemorrhage or
myocardial infarction),
●metabolic disorders
(diabetic acidosis,
hypoglycemia, uremia,
hepatic coma,
addisonian crisis,
electrolyte imbalance),
●intoxication (with
alcohol, barbiturates,
narcotics, bromides,
analgesics, carbon
monoxide, heavy
metals),
●miscellaneous
disorders
(hyperthermia,
hypothermia, severe
systemic infections)

Stupor and obtundation are still lesser grades of depressed consciousness and are characterized by
variable degrees of impaired reactivity. Acute confusional states must be distinguished from coma or
dementia

Sleep-wake mechanism
The alternation of circadian cycle effects the Hormone release, eating habits and digestion and body temperature.
In biological function:
1. At the start of the day, the transcription of Clk and Bmal1 commencences, and the proteins CLOCK (C) and
BMAL1 (B) are synthesized in tandem.
2. When the C and B protein are sufficient, then forms the dimers and the DNA sequence in the cytoplasm
3. This then act as a circadian transcriptional enhancers of the genes Cry, Per 1, 2, and 3 and CCG -> which can
be form back in the nucleus
4. CRY binds to C-B dimers, by the stimulation from PER2 -> this allows the inhibition of other genes
 5. This feedback loop, tooks 24 hours
circadian clocks evolved to maintain appropriate periods of sleep and wakefulness (amount of daylight and
darkness in different seasons and at different places on the planet).
1. In order to do this, the biological clock must detect decreases in light levels as night approaches
a. The receptors that detect the changes are the retina, and not the rods and cones
2. Suprachiasmatic nucleus (SCN) -> located in the hypothalamus (the site of the circadian control of
homeostatic functions, such as: synchronized with the sleep-wake cycle, including body temperature,
hormone secretion, urine production, and changes in blood pressure)
3. In the activation of SCN, there is a need for the response of the axon, which are preganglionic (link visceral
motor neurons in spinal cord and brainstem to autonomic ganglia) sympathetic neurons in the lateral horn
of the spinal cord
4. The pineal gland synthesizes the sleep promoting neurohormone melatonin from tryptophan, and secretes
it into the bloodstream to help alternate the brainstem circuits to start the sleep-wake cycle
5. Melatonin increases, when the light sufficiency decreases, that means by 2:00 and 4:00 a.m, the melatonin
production increases.
In elderly people, they are more prone to insomnia or sleep lesser compare to younger people, because the pineal
gland calcifies and less melatonin is produced

Sleep
1. Periodicity
The daily cycle of the arousal, which determines the sleep and wake system in the body, which is
regulated by the reticular formation structures in the hypothalamus and the brain stem.
The sleep process happens in the 24 hours of the circadian rhythm, that presents the turn off of the
neural activity. However, the physiological function is still active. The nerve cells in the reticular
formation from the pons release just before sleep. Lesions of the pons just forward of the trigeminal
nerve produce a state of hyperalertness and much less sleep than normal.
2. Stages
The sleep cycle takes in about 90 minutes. There are two types:
● slow-wave sleep
○ Stage 1 of slow-wave (spindle) sleep is characterized by easy arousal
○ Stages 2 to 4 are progressively deeper, and the electroencephalographic pattern
becomes more synchronized
○ Stage 4 can be considered the deepest stage, which means that blood pressure, pulse
rate, respiratory rate, and the amount of oxygen consumed by the brain are very low
● rapid eye movement (REM) sleep
○ characterized by the sudden appearance of an asynchronous pattern on
electroencephalograms. The sleepers show a striking loss of muscle tone in the limbs,
and have vivid visual imagery and complex dreams. There is a specific need for REM
sleep, which is triggered by neurons in the dorsal midbrain and pontine tegmentum.

The midline raphe system of the pons may be responsible for bringing on sleep; it may act through the
secretion of serotonin, which modifies many of the effects of the reticular activating system. Paradoxic REM
sleep follows when a second secretion (norepinephrine), produced by the locus ceruleus, supplants the raphe
secretion. The effects resemble normal wakefulness.
Destruction of the rostral reticular nucleus of the pons abolishes REM sleep, usually without affecting
slow-wave sleep or arousal. REM sleep is suppressed by dopa or monoamine oxidase inhibitors, which
increase the norepinephrine concentration in the brain. Lesions of the raphe nuclei in the pons cause
prolonged wakefulness.

2. Jelaskan etiologi patofisiologi terhadap penurnuan kesadaran

 ● Syncope -> the transient loss of consciousness due to the postural tone dues to the reduced cerebral
blood flow
○ Etiology
■ Cardiogenic
● There is lesion or structural abnormalities of the heart
● There is cardiac arrhythmias (which can be either brady cardia or tachycardia)

● This leads to the decrease cardiac output

■ Neurocardiogenic
● Known to be vasovagal syncope
● Caused by pain, fear, anxiety, close quarters and excessive heat
● The most common cause of syncope
■ Metabollic
○ Pathophysiology

Impaired consciousness is caused by various etiological factors, both intracranial and extracranial/systemic. A
brief explanation of the etiological factors of impaired consciousness are as follows:
a. Disorders of blood circulation in the brain (cerebrum, cerebellum, or brainstem)
- Bleeding, thrombosis or embolism
- Considering the high incidence of stroke, it is necessary to underline the suspicion of stroke in any event of
impaired consciousness.
b. Infections: encephalomeningitis (meningitis, encephalitis, cerebritis/brain abscess) - Considering that
infection (bacteria, viruses, fungi) is a common disease in Indonesia, any disturbance of consciousness
accompanied by elevated body temperature should be suspected of having encephalomeningitis.
c. Metabolic disorders
- In Indonesia, liver disease, kidney failure, and diabetes mellitus are common.
d. Neoplasm
- Brain neoplasms, both primary and metastatic, are common in Indonesia.
Neoplasms are more common in adults and the elderly.
- Decreased consciousness generally occurs gradually but progressive / not acute.
e. Head trauma
- Head trauma is most often caused by traffic accidents.
f. Epilepsy
- Impaired consciousness occurs in cases of generalized epilepsy and status epilepticus
g. Intoxication
- Intoxication can be caused by drugs, poisons (suicide attempts), certain foods and other chemicals.
h. Electrolyte and endocrine disorders
- This disorder often does not show its “identity” clearly; thus requires special attention so as not to be
forgotten in any search for the cause of the disturbance of consciousness.

3. Jelaskan pemeriksaan pada pasien dengan kehilangan kesadaran

All about seizure and syncope

Syncope Seizure

Definition a transient, self-limited loss of

consciousness due to acute global
impairment of cerebral blood flow.

Onset rapid, duration brief, and recovery

spontaneous and complete

Causes (1) neurally mediated syncope (also

called reflex or vasovagal syncope),
(2) orthostatic hypotension
(3) cardiac syncope

● syncopal prodrome (presyncope) is

common -> can be unconscious
without warning
● Typical presyncopal symptoms
include dizziness, lightheadedness
or faintness, weakness, fatigue, and
visual and auditory disturbances.

Similar, but need to seizures, vertebrobasilar ischemia,

differentiate hypoxemia, and hypoglycemia

Epidemiology ● The incidence is slightly higher in

females than males
● In young subjects, there is often a
family history in first-degree
relatives.
DDx ● seizures,
● vertebrobasilar ischemia,
● hypoxemia,
● hypoglycemia

Categories

Natural history ● If this is the first seizure, then the

emphasis will be to:
● (1) establish whether the reported
episode was a seizure rather than
another paroxysmal event
● (2) determine the cause of the seizure
by identifying risk factors and
precipitating events
● (3) decide whether anticonvulsant
therapy is required in addition to
treatment for any underlying illness

It mainly focuses on the risk factors (

prior head trauma, stroke, tumor, or CNS
infection should be identified) and
predisposing events (a history of febrile
seizures, a family history of seizures,
and, of particular importance, earlier
auras or brief seizures not recognized).

Physical exmination ● If this is the first seizure, then the

emphasis will be to:
● (1) establish whether the reported
episode was a seizure rather than
another paroxysmal event
● (2) determine the cause of the seizure
by identifying risk factors and
precipitating events
● (3) decide whether anticonvulsant
therapy is required in addition to
treatment for any underlying illness

Lab ● identify the more common metabolic

causes of seizures such as
abnormalities in electrolytes, glucose,
calcium, or magnesium, and hepatic
or renal disease

Classification

Laboratory test ● Baseline laboratory blood tests are

rarely helpful in identifying the
cause of syncope. Blood tests
should be performed when specific
disorders, e.g., myocardial
infarction, anemia, and secondary
 autonomic failure, are suspected

Treatment ● Reassurance, avoidance of

provocative stimuli, and plasma
volume expansion with fluid and salt
are the cornerstones of the
management of neurally mediated
syncope.
● Isometric counterpressure
maneuvers of the limbs (leg
crossing or handgrip and arm
tensing) may raise blood pressure
by increasing central blood volume
and cardiac output. -> maintaining
pressure in the autoregulatory zone,
these maneuvers avoid or delay the
onset of syncope.
● Fludrocortisone, vasoconstricting
agents, and β-adrenoreceptor
antagonists -> can be beneficial to
treat the refractory patients
● Patients That age > 40 years
(syncope is associated with asystole
or severe bradycardia and patients
with prominent cardioinhibition due
to carotid sinus syndrome)

Prognosis ● The prognosis after a single

syncopal event for all age groups is
generally benign. In particular,
syncope of noncardiac and
unexplained origin in younger
individuals has an excellent
prognosis; life expectancy is
unaffected
● By contrast, syncope due to a
cardiac cause, either structural
heart disease or primary arrhythmic
disease, is associated with an
increased risk of sudden cardiac
death and mortality from other
causes
● Similarly, mortality rate is increased
in individuals with syncope due to
orthostatic hypotension related to
age and the associated comorbid
conditions

Syncope Loss of consciousness

A sudden transient loss of consciousness and Occurs within 10 seconds of hypoperfusion of the
postural tone with spontaneous recovery reticular activating system in the midbrain
All about TBI

Traumatic Brain Injury (TBI)

Definition an alteration in brain function, or other evidence of brain pathology, caused by an

external force, and characterized by the following:
 (1) any period of loss or decreased level of consciousness (LOC),
(2) any loss of memory for events immediately before (retrograde) or after
(posttraumatic) the injury,
(3) any neurological deficits, and/or
(4) any alteration in mental state at the time of injury.

Mechanism ● head being struck by an object, the head striking an object,

● the brain undergoing an acceleration/deceleration movement,
● a foreign body penetrating the brain, or
● forces generated from events such as a blast or explosion

injury Glasgow coma scale (eye, verbal, motor, e.g., E3V4M6); total score of 13
classification
systems

● (GCS 13–15) - normal

● (GCS 9–12) - moderate
● (GCS 3–8) - Severe

TBI TYPES AND Mild TBI (Concussion): between 70 and 90% of all treated traumatic brain injuries are
PATHOLOGIES mild in severity based on traditional case definitions and acute injury characteristics,
with most reported estimates in the order of 85%

● Skull Fracture
● skull that exceeds the elastic tolerance of the bone causes a fracture
● increases many-fold the chances of an underlying subdural or epidural hematoma
● If the arachoid membrane is affected, then there is chance bacteria to the
cerebrospinal fluid (CSF) with a risk of meningitis and for leakage of CSF outward
through the dura. If there is leakage, then severe orthostatic headache results from
lowered pressure in the spinal fluid compartment
● SIGNS: Hemotympanum (blood behind the tympanic membrane), ecchymosis over
the mastoid process (Battle sign), and periorbital ecchymosis (“raccoon sign”) are
associated with basilar fractures and should be suspected if these clinical signs are
present.

● Epidural Hematoma: Hemorrhages between the dura and skull

● an injury to a meningeal arterial vessel and evolve rapidly
● 10% of cases of severe head injury
● Rapid surgical evacuation and ligation or cautery of the damaged vessel, usually the
middle meningeal artery that has been lacerated by an overlying skull fracture, is
indicated. If recognized and treated rapidly, patients often have a favorable outcome.

● Acute Subdural Hematoma: Hemorrhages beneath the dura

● May be minor, but due to acceleration forces, can accidentally produce one
● most are drowsy or comatose from the moment of injury
● A unilateral headache and slightly enlarged pupil on the side of the hematoma are
frequently
● Might require surgery

● Chronic Subdural Hematoma

● From an acute and evolve to days or weeks after injury with drowsiness, headache,
confusion, or mild hemiparesis, usually in the elderly with age-related atrophy and
often after only minor or unnoticed trauma
● Headache is common but not invariable
● Additional features that may appear weeks later include slowed thinking, vague
change in personality, seizure, or a mild hemiparesis
● CT without contrast initially shows a low-density mass over the convexity of the
hemisphere. Between 2 and 6 weeks after the initial bleeding, the clot becomes
isodense compared to adjacent brain and may be inapparent
● Treatment with surgical evacuation through burr holes is usually successful, if a
cranial drain is used postoperatively

● TRAUMATIC SUBARACHNOID HEMORRHAGE: Rupture of small cortical arteries

or veins can cause bleeding into the subarachnoid space, and it is quite common in
the TBI
● WHich can be seen into 2, there are Contusion and Axonal Injury

● Contusion: A surface bruise of the brain, or contusion, consists of varying degrees of

petechial hemorrhage, edema, and tissue destruction
● This happens through the mechanism forces that displace and compress the
hemispheres forcefully and by deceleration of the brain against the inner skull, either
under a point of impact (coup lesion) or, as the brain swings back, in the antipolar
area (contrecoup lesion.
● clinical signs of contusion are determined by the location and size of the lesion;
often, there are no focal abnormalities with a routine
● these injured regions are later the sites of gliotic scars that may produce seizures
● Contusions in the temporal lobe may cause delirium or an aggressive, combative
syndrome
● Acute contusions are easily visible on CT and MRI scans; can be located in the
hyperintense on T2
● Blood in the CSF due to trauma may provoke a mild inflammatory reaction

● Axonal Injury
● Another common injury after TBI
● It occurs following high-speed deceleration injuries, such as motor vehicle collisions
● usually in the corpus callosum and centrum semiovale -> located in the CT scan

● CRANIAL NERVE INJURIES

● are the olfactory, optic, oculomotor, and trochlear; the first and second branches of
the trigeminal nerve; and the facial and auditory nerves
● Anosmia and an apparent loss of taste (actually a loss of perception of aromatic
flavors, with retained elementary taste perception) occur in ~10% of persons with
serious head injuries, particularly from falls on the back of the head.
● Diplopia limited to downward gaze and corrected when the head is tilted away from
the side of the affected eye indicates trochlear (fourth nerve) nerve damage
● Facial nerve injury caused by a basilar fracture is present immediately in up to 3%
of severe injuries; it may also be delayed for 5–7 days
● Delayed facial palsy occurring up to a week after injury, the mechanism of which is
unknown, has a good prognosis.
● Injury to the eighth cranial nerve from a fracture of the petrous bone causes loss
of hearing, vertigo, and nystagmus immediately after injury
● Deafness from eighth nerve injury is rare and must be distinguished from blood in
the middle ear or disruption of the middle ear ossicles
● Dizziness, tinnitus, and high-tone hearing loss occur from cochlear concussion

● SEIZURE: brief period of tonic extensor posturing or a few clonic movements of the
limbs just after the moment of impact can occur
 ● Convulsions are surprisingly uncommon immediately after TBI
● However, the cortical scars that evolve from contusions are highly epileptogenic
and may later manifest as seizures, even after many months or years
● Penetrating injuries have a much higher rate of subsequent epilepsy

Clinical syndrome CONCUSSION/MILD TBI

and Treatment ● Briefly lost consciousness or been stunned after a minor head injury usually
becomes fully alert and attentive within minutes but may complain of headache,
dizziness, faintness, nausea, a single episode of emesis, difficulty with
concentration, a brief amnestic period, or slight blurring of vision.
● This is good prognosis with little risk of subsequent deterioration
● Children are particularly prone to drowsiness, vomiting, and irritability,
symptoms that are sometimes delayed for several hours after apparently minor
injuries. Generalized or frontal headache is common in the following days
● The patient can go home after several hours of observation, and must be back if the
patient’s condition becomes worse
● Persistent severe headache and repeated vomiting in the context of normal
alertness and no focal neurologic signs is usually benign, but CT should be obtained
and a longer period of observation is appropriate
● The decision to perform imaging tests also depends on clinical signs that indicate
that the impact was severe (e.g., persistent confusion, repeated vomiting, palpable
skull fracture)
● Guidelines have also indicated that older age (>65), two or more episodes of
vomiting, >30 min of retrograde or persistent anterograde amnesia, seizure,
and concurrent drug or alcohol intoxication are sensitive (but not specific) indicators
of intracranial hemorrhage that justify CT scanning.

SPORT-RELATED CONCUSSION
● Concussion is a frequent injury in contact and collision sports
● The chance of recovery also can be within 1 week, and be discharged from
Emergency department
● majority of athletes achieve a complete recovery in symptoms, cognitive functioning,
postural stability, and other functional impairments over a period of 1–3 weeks
following concussion

POSTCONCUSSIVE STATES
● A minor TBI
● consisting of combinations of fatigue, dizziness, headache, and difficulty in
concentration
● Headache may initially be treated with acetaminophen and small doses of
amitriptyline
● Vestibular exercises and small doses of vestibular suppressants such as
promethazine (Phenergan) may be helpful when dizziness is the main problem.
● In addition, patients are frequently referred to behavioral health providers such as
neuropsychologists, rehabilitation psychologists, health psychologists, and/or
psychiatrists for a variety of reasons, but particularly when they are experiencing
cognitive, emotional, or behavioral changes that accompany PCD.
● Patients with mood disorders (e.g., depression), anxiety disorders (e.g.,
posttraumatic stress disorder), or adjustment reactions may benefit from psychiatric
consultation for appropriate medication trials or from time-limited psychotherapy
such as cognitive behavioral therapy.

INJURY OF INTERMEDIATE SEVERITY

● Patients who are not fully alert or have persistent confusion, behavioral changes,
extreme dizziness, or focal neurologic signs such as hemiparesis should be
admitted to the hospital and undergo a cerebral imaging study
● Common syndromes include:
● (1) delirium with a disinclination to be examined or moved, expletive speech, and
resistance if disturbed (anterior temporal lobe contusions);
● (2) a quiet, disinterested, slowed mental state (abulia) alternating with irascibility
(inferior frontal and frontopolar contusions);
● (3) a focal deficit such as aphasia or mild hemiparesis (due to subdural
hematoma or convexity contusion or, less often, carotid artery dissection);
● (4) confusion and inattention, poor performance on simple mental tasks, and
fluctuating orientation (associated with several types of injuries, including those
described above, and with medial frontal contusions and interhemispheric subdural
hematoma);
● (5) repetitive vomiting, nystagmus, drowsiness, and unsteadiness (labyrinthine
concussion, but occasionally due to a posterior fossa subdural hematoma or
vertebral artery dissection); and
● (6) diabetes insipidus (damage to the median eminence of pituitary stalk).
● Injuries of this degree are often complicated by drug or alcohol intoxication, and
clinically inappropriate cervical spine injury may be present.

● After surgical removal of hematomas, patients in this category improve over weeks
to months
● During the first week, the state of alertness, memory, and other cognitive
functions often fluctuate, and agitation and somnolence are common.
Behavioral changes tend to be worse at night, as with many other
encephalopathies, and may be treated with small doses of antipsychotic
medications. Subtle abnormalities of attention, intellect, spontaneity, and memory
return toward normal weeks or months after the injury, sometimes abruptly.
However, the full extent of recovery may not be realized for several years.

SEVERE INJURY
● Patients who are comatose from the moment of injury require immediate neurologic
attention and resuscitation.
● After intubation, with care taken to immobilize the cervical spine, the depth of
coma, pupillary size and reactivity, limb movements, and Babinski responses
are assessed.
● As soon as vital functions permit and cervical spine x-rays and a CT scan have been
obtained, the patient should be transported to a critical care unit.
● Hypoxia should be reversed, and normal saline used as the resuscitation fluid in
preference to albumin
● the finding of an epidural or subdural hematoma or large intracerebral
hemorrhage is usually an indication for prompt surgery and intracranial
decompression in an otherwise salvageable patient
● Measurement of ICP with a ventricular catheter or fiber optic device in order to
guide treatment has been favored by many units but has not improved outcome.
Hyperosmolar intravenous solutions are used in various regimens to limit
intracranial pressure. Prophylactic antiepileptic medications are recommended for 7
days and should be discontinued unless there are multiple seizures postinjury
● The recovery from severe TBI can take years
● Recent best practice guidelines recommend, in the absence of brain death, that
aggressive therapy be instituted for at least 72 h in the acute injury period.
Pathophysiology of TBI [Emergency medicine, comprehensive study]

disruption of the neurochemical homeostasis, and loss of the electrochemical function. direct damage to, or the
breakdown of, the blood–brain barrier, ionic shifts, and alteration of water exchange mechanisms (e.g.,
aquaporins). As intracellular and extracellular water content rises, the brain swells and the ICP increases,
leading to direct compressive tissue damage, vascular compression-induced ischemia, brain parenchyma
herniation, and brain death.