ASSESSMENT OF CONSCIOUSNESS BY MEANS OF GLASGOW

COMA SCALE

1974 Teasdale and Jenett Attempt to bring uniformity to the clinical

examination and clinical communication about the level of consciousness

GCS Not designed to capture distinct details

of the neurologic examination

The ascending reticular activating system (ARAS) is a network of neurons originating in the tegmentum of the upper pons and midbrain, believed to be integral to inducing and maintaining alertness. These neurons project to structures in the diencephalon, including the thalamus and hypothalamus, and from there to the cerebral cortex. Alterations in alertness can be produced by focal lesions within the upper brainstem by directly damaging the ARAS.

Injury to the cerebral hemispheres can also produce coma, but in this case, the involvement is necessarily bilateral and diffuse, or if unilateral, large enough to exert remote effects on the contralateral hemisphere or brainstem. Magnetic resonance imaging (MRI) studies have indicated that coma in supratentorial mass lesions occurs both with lateral forces on the contralateral hemisphere and with downward, brainstem compression

The GCS is universally accepted as a tool for TBI classification because of its simplicity, reproducibility, and predictive value for overall prognosis. However, it is limited by confounding factors such as medical sedation and paralysis, endotracheal intubation, and intoxication. These confounding issues are often particularly prominent in patients with a low GCS score

The GCS is not useful for the diagnosis of coma

An alternative scoring system, the Full Outline of Unresponsiveness (FOUR) Score, has been developed in order to attempt to obviate these issues, primarily by including a brainstem examination. However, this lacks the long track record of the GCS in predicting prognosis and is somewhat more complicated to perform, which may be a barrier for nonneurologists

The most commonly used scale is the Glasgow Coma Scale (GCS). Although the originators of the GCS have reported data on practical reliability of the scale, other studies have showed some difficulties in application by untrained nursing staff. Trained personnel tend to apply the GCS better, although interpretation of intermediate scores on the GCS remains difficult for emergency physician.

Other shortcomings of the GCS have been recognized.

1. because many comatose patients are intubated, the verbal component cannot be tested. Some clinicians use the lowest possible score; others extrapolate the verbal response based on other neurological findings.

2. abnormal brainstem reflexes, changing breathing patterns, and the need for mechanical ventilation could reflect severity of coma, but the GCS does not include those clinical indicators.

3. The GCS may not detect subtle changes in neurological examination.

4. More recently, a study in traumatic head injury found lack of correlation between outcome and GCS score.

An alternative scoring system, the Full Outline of Unresponsiveness (FOUR) Score, has been developed in order to attempt to obviate these issues, primarily by including a brainstem examination

The FOUR score has four testable components, in contrast with the GCS. The number of components and the maximal grade in each of the categories is four (E4, M4, B4, R4). (It is easier to remember than the GCS with its varying number of scores [E4, M6, V5]

FOUR Score

HEAD INJURIES (3B)

INTRODUCTION

 Traumatic brain injury (TBI) is the leading cause of death in North America for individuals between the ages of 1 and 45. Many survivors live with significant disabilities, resulting in major socioeconomic burden as well. In 2000, the economic impact of TBI in the United States was estimated to be $9.2 billion in lifetime medical costs and $51.2 billion in productivity losses

EPIDEMIOLOGY

The overall incidence of TBI in the United States was estimated to be 538.2 per 100,000 population, or around 1.5 million new cases in 2003. Somewhat lower rates are reported in Europe (235 per 100,000) and Australia (322 per 100,000)

EPIDEMIOLOGY Rates of TBI are highest in the very young (age

group zero to four years) and in adolescents and young adults (15 to 24 years); there is another peak in incidence in the elderly (age >65 years). Approximately 78 percent of TBI are treated in the emergency department only; 19 percent of patients require hospitalization, and 3 percent are fatal. Most cases treated in emergency departments occur in the very young (ages zero to four years), while hospitalization rates are highest in patients older than 65 years.

EPIDEMIOLOGY

As with most traumatic injuries, the incidence of TBI is significantly higher in men compared to women, with ratios that vary between 2.0 to 1 and 2.8 to 1. For severe TBI, the gender ratio is more pronounced, 3.5 to 1. Lower socioeconomic status is also a risk factor for head injury.

EPIDEMIOLOGY Falls are the leading cause of TBI (particularly

in older patients), followed by motor vehicle accidents. The proportion of TBI secondary to violence has risen over the past decade and now accounts for 7 to 10 percent of cases. TBI related to military combat has received increased attention in the years from 2002 to 2009. Mechanistic aspects of combat-related trauma may differ from TBI related to other causes, as the former usually involve blast explosives.

EPIDEMIOLOGY

Moderate and severe TBIs are associated with neurologic and functional impairments. The prevalence of long-term disability related to TBI in the United States is variably estimated to be between 3.2 to 5.3 million, or approximately 1 to 2 percent of the population.

EPIDEMIOLOGI

Di USA terjadi 2 juta CK/tahun & 1 CK/15 detik; 500.000 dirawat di RS; 1 meninggal & 1 cacat tiap 5 menit. Kecelakaan lalu lintas 51%; jatuh 21%; kekerasan 12% & Olah raga 12%. Di RSUPN Ciptomangunkusumo Jakarta CK menduduki peringkat pertama. Di RSUP Dr. Sardjito Jogjakarta, menduduki 3 besar.

CLASSIFICATION

 TBI is a heterogeneous disease. There are many different ways to categorize patients in terms of clinical severity, mechanism of injury, and pathophysiology, each of which may impact prognosis and treatment.

CLASSIFICATION

The best prognostic models ideally include all of the factors described below, as well as age, medical comorbidity, and laboratory parameters. However, treatment decisions are likely best informed by considering these variables individually rather than as a lump score. Further efforts at improved classification are ongoing as these may help to refine treatment approaches

CLASSIFICATION OF TBI BY MECHANISM

Closed/blunt force—injury caused by direct force to head, acceleration/deceleration, or rotational forces. Common causes include falls, assault, and motor vehicle collisions.

Blast injury—injury caused by overpressure waves generated from high grade explosives.

Penetrating injury—injury induced by an object that penetrates the cranial vault. Common causes include gunshot wounds, shrapnel, and knife wounds.

Penetrating Head Injury : Gunshot Wound

Penetrating Head Injury : Stab Injury

Stab to right temporal region. Knife passing behind orbit ending in nasopharynx.

STRUCTURALLY BASED DESCRIPTIONS OF TBI Epidural/extradural hematoma (EDH) Subdural hematoma (SDH) Traumatic axonal injury (TAI, also referred to as diffuse

axonal injury, or DAI)

Traumatic subarachnoid hemorrhage (TSAH or SAH) Intraventricular hemorrhage (IVH), IVH is typically seen

in conjunction with TSAH Contusion-parenchymal

hemorrhage, typically in frontal or temporal lobes. Coup injuryContre coup injury

Skull fractures

STRUCTURALLY BASED DESCRIPTIONS OF TBI

Epidural/extradural hematoma (EDH) Subdural hematoma (SDH) Traumatic axonal injury (TAI, also referred to as

diffuse axonal injury, or DAI) Traumatic subarachnoid hemorrhage (TSAH or

SAH) Intraventricular hemorrhage (IVH), IVH is typically

seen in conjunction with TSAH Contusion - parenchymal hemorrhage, typically in

frontal or temporal lobes. Contusions may be “coup” or “contre coup”

Skull fractures

Epidural/extradural hematoma

STRUCTURALLY BASED DESCRIPTIONS OF TBI

EDH SDH DAI

TSAH

Contusion

IVH

CONCUSSION

It is altered mental state occurring after trauma, which may or may not include loss of consciousness. Symptoms reflect a functional disturbance rather than structural injury. The American Academy of Neurology (AAN) concussion grading scale has been widely used to describe the severity of concussion

Practice Parameter: The management of concussion in sports (summary statement). Neurology. 1997;48:581–585

AAN Practice Parameter Grading System for Concussion

Klasifikasi : Patofisiologi

Komosio serebri : jaringan otak tidak rusak hanya kehilangan fungsi sesaat, pingsan < 10’ atau amnesia

kontusio serebri : kerusakan jaringan otak + defisit neurologik, pingsan > 10’

laserasi otak : kerusakan otak luas & jaringan otak robek sering dengan fraktur

Clinical severity scores

TBI has traditionally been classified using injury severity scores; the most commonly used is the Glasgow Coma Scale (GCS). A GCS score of 13 to 15 is considered mild injury, 9 to 12 is considered moderate injury, and 8 or less as severe traumatic brain injury.

The GCS is universally accepted as a tool for TBI classification because of its simplicity, reproducibility, and predictive value for overall prognosis. However, it is limited by confounding factors such as medical sedation and paralysis, endotracheal intubation, and intoxication. These confounding issues are often particularly prominent in patients with a low GCS score

Klasifikasi : tingkat kesadaran

Cedera kepala ringan (CKR) : GCS 13-15

Cedera kepala sedang (CKS): GCS 9-12

Cedera kepala berat (CKB) : GCS 3-8

Perdarahan intrakranial dengan GCS CKR atau CKS dianggap sebagai CKS

Classification - GCS Eyes

4 opens spontaneously

3 opens to verbal2 opens to pain1 do not open

Verbal5 oriented4 confused3 inappropriate2 incomprehensible1 none

Motor6 obeys5 localizes4 withdraws3 abnormal flex2 extensor response1 none

ScoringMild >12Moderate 9-12Severe <9

Classification - GCS - Mortality

Developed for prognosis in severe TBI

Timing of score is not standardized One score not sufficient - perform

serial examsPrognosis worse if score does not

improve or if it worsens Does not account for drugs, seizures,

or metabolic problems

Classification - GCS - Mortality

Severe = 40%3 = 80%4 = 55%5 = 40%

Moderate = 12% Mild = 01%

Glasgow Outcome Scale

Rancho Los Amigos Level of Cognitive Functioning

The Rancho Scale is widely used by rehabilitation facilities after the patient leaves the neurosurgical intensive care unit or neurosurgical

floor for postacute care

PATHOPHYSIOLOGY

The pathophysiology of TBI-related brain injury is divided into two separate but related categories:

1. primary brain injury and

2. secondary brain injury

Primary brain Injury

Primary brain injury occurs at the time of trauma. Common mechanisms include direct impact, rapid acceleration/deceleration, penetrating injury, and blast waves. Although these mechanisms are heterogeneous, they all result from external mechanical forces transferred to intracranial contents. The damage that results includes a combination of focal contusions and hematomas, as well as shearing of white matter tracts (diffuse axonal injury) along with cerebral edema and swelling.

Secondary brain Injury

Secondary brain injury in TBI is usually considered as a cascade of molecular injury mechanisms that are initiated at the time of initial trauma and continue for hours or days. These mechanisms include :

- Neurotransmitter-mediated excitotoxicity causing glutamate, free-radical injury to cell membranes

- Secondary ischemia from vasospasm, focal microvascular occlusion, vascular injury

- Electrolyte imbalances - Mitochondrial dysfunction

 -Inflammatory responses - Apoptosis

 

MASALAH

Tidak ada akses dan informasi medik di tempat kejadian (on-site) Angka kematian terbesar di lokasi kejadian ( > 50%) Kualitas klinis yang sampai di RS tergantung keberhasilan resusitasi di tempat kejadian/ selama perjalanan Lama transportasi ke RS terdekat dapat merupakan faktor penentu kualitas klinis

PRIMARY SURVEY

HYPOXEMIA

HYPEROXEMIA

PAO2 80 – 120PACO2 25 – 35

PREVENTAB

BPC

Systole : 100 – 140 mmHg

Diastole : 70 – 90 mmHg

• Hypertension• Hypotension• Shock• Anemia

UrgencyImmediately

Treated

Blunt Head Injury

Periorbital haematoma ('panda eyes') suggestive of basal skull fracture.

Cedera sekunder dari hematoma epidural (panah kosong). Tampak pergeseran fissura sylvi ke inferior (1), herniasi subfalcine dengan kompresi ventrikel ipsilateral (2), dilatasi ventrikel kontralateral akibat obstruksi fungsional pada foramen Monro (3), arteri serebri anterior menyeberangi midline (4), kontusio midbrain (5), perdarahan midbrain Duret akibat pergeseran ke bawah (6), herniasi lobus temporal medial melewati insisura tentorial (7), kompresi arteri serebri posterior ipsilateral (8), pelebaran sisterna CPA ipsilateral (9), herniasi tonsilar (10).

OBSERVATION

PATIENT

ARTIFICIAL RESP.

Cushing Response

Neurologic Signs : Pupil, Motoric

WITHOUT

GCS

Cushing Response

Neurologic Signs

Skull X Ray

Head CT Scan

Head MRI

Cervical X Ray

IMAGING :

Skull X RAY INDICATIONS

* Open fracture

* Deformity

* Stab wound

* Corpus alienum

* Scraped wound

BRAIN INJURY

A B C

DIAGNOSTIC

MANAGEMENT

PBI

SCI

RECOVERPREVENT

TREAT

Boor Hole ExplorationImaging

12 POINTS

OPERATIVE CONSERVATIFE

Clinical signs* GCS* Vital Signs* Neurological signs

CERVICAL SPINE X RAY INDICATIONS

* Scraped wound on the neck

* Neck pain

* Traumatic mechanism ( wisplash injury )

* Cervical signs : tetra plegia / paralytis

* Unconscious patients

CT SCAN INDICATIONS

* Seizures

* Continuous cephalgi, vomiting and vertigo with medicine

* Corpus alienum or stab wound

* GCS < 15

* Lateralization ( anisocor / hemiparalysis )

* Decreased of GCS > 1 point

* Cushing response : hypertension + bradicardy

* Brain + multiple organ injury

* Social indication

CT scan - CKR Di Amerika Utara berkembang 3 pendapat tentang perlu

tidaknya dilakukan CT scan kepala. Pendapat pertama, yang sebagian besar terdiri dari ahli bedah

saraf, merekomendasikan pemeriksaan CT scan kepala pada semua pasien CK dengan penurunan kesadaran atau amnesia walaupun pemeriksaan fisik normal, The American College of Surgeons menyatakan kecuali pada pasien dengan CK sangat ringan, semua pasien CK memerlukan pemeriksaan CT scan kepala

Pendapat kedua, yang terdiri dari ahli bedah saraf, dokter instalasi rawat darurat dan ahli radiologi, merekomendasikan pendekatan yang selektif pemakaian CT scan kepala pada CKR.

Sedangkan pendapat ketiga memberikan rekomendasi yang tidak jelas pemakaian CT scan kepala pada CKR dan menyatakan diperlukan penelitian lebih lanjut

Use of CT in Diagnosing MTBI Retrospective study, 215 hospitalized patients

Mild TBI without complications Mild TBI with complications (positive CT) Moderate TBI

Mild TBI patients with positive CT performed on neuropsychiatric testing like moderate TBI

Moderate group had worse function at 6 months Length of LOC or amnesia did not differentiate

mild from moderate groups Depressed skull fractures without parenchymal

lesions performed as mild TBI

Williams et al. Neurosurgery 1990;27:422.

Skull Radiographs and Intracranial Lesions

Retrospective review 207 hospitalized patients with

intracranial lesions 63% had no skull fracture Skull films do not predict

intracranial lesion

Cooper P, Ho V. Neurosurgery 1983;13:136

Retrospective review 22,058 cases Patients with skull fractures, 91% did not

have intracranial injury 51% of patients with intracranial injury

did not have a skull fracture

Masters et al. NEJM 1987;316:84-91

Skull Radiographs and Intracranial Lesions

Skull Radiographs and Intracranial Lesions

Prospective study: 7035 patients Not all patients received same tests48% lost to follow-up

Skull fracture did not predict an intracranial injury

Absence of a skull fracture did not rule out an intracranial injury

Plain films are neither sensitive nor specific for intracranial injury

Masters et al. NEJM 1987;316:84-91

FRAKTUR

Fraktur linier umumnya lurus atau membentuk kurva. Kadangkala dapat dijumpai angulasi dan percabangan dari fraktur (panah), seperti pada gambar dimana fraktur tulang frontal juga disertai dengan fraktur sinus frontalis.

Fraktur linier kominutif (tanda panah) di daerah frontal dan

sfenoid. Perhatikan juga adanya pneumosefalus dan gas-fluid level

di sinus sfenoid.

Fraktur linier tulang temporal (panah). Garis fraktur lebih kehitaman, tidak keabuan. Seringkali disalah artikan

dengan jejas vaskuler meningeal.

Fraktur diastatik. Pada proyeksi AP tampak garis fraktur di oksipital kiri yang meluas ke sutura sagitalis dengan disertai diastasis dari sutura.

Fraktur depresi kominutif dengan garis fraktur multipel yang radial. Pada proyeksi lateral tampak garis frakturkurvilinier. Tampak garis peningkatan densitas,

menandakan suatu fraktur depresi, akibat superimposisi tepi tulang (panah hitam). Tampak juga garis fraktur dengan densitas yang lebih rendah, juga merupakan fraktur depresi tetapi tepi tulang terpisah dan tidak ada superimposisi (panah

kosong). Pada proyeksi frontal, tampak fragmen-fragmen depresi tulang .

Fraktur depresi yang terlihat pada proyeksi tangensial (kanan) dan proyeksi lateral (bawah).

Low Risk Group For Intracranial Injury

Asymptomatic Headache Dizziness Scalp hematoma, laceration,

contusion Absence of LOC or amnesia No patients with neurologic

deterioration identified No imaging study indicated

Masters et al. NEJM 1987;316:84-91

Moderate Risk Group For Intracranial Injury

Loss of consciousness Unreliable history Progressive headache Alcohol or drug intoxication Age less than 2 years Post traumatic seizure BSF / multiple trauma / possible

penetrating trauma CT scan recommended

Masters et al. NEJM 1987;316:84-91

Head CT In Mild TBI Retrospective review 1538 trauma admissions GCS > 12; all with history of LOC or amnesia 265 (17.2%) had intracranial lesion:

GCS 13: 37.5%GCS 14: 24.2%GCS 15: 13.2%

58 (3.8% of total 22% of patients with positive CT) required neurosurgery

No patient with a normal CT deteriorated

Stein S, Ross S. Ann Emerg Med 1993;22:1193

Head CT In Mild TBI Prospective study: 712 consecutive ED

patients GCS 15; history of LOC or amnesia Nonfocal neurologic exam

4 object recall and digit span testing 67 (9.4%) had a positive head CT 2 (.28%) required emergent neurosurgery No statistical model could be created to

classify 95% of patients into CT normal vs abnormal

Jeret et al. Neurosurgery 1993;32:9

Head CT in Mild TBI Prospective study in patients with a GCS of 15 Phase 1: 520 patients to create 7 criteria:

(headache, vomiting, age over 60, intoxication, memory deficits, evidence of trauma, seizure)

Phase 2: 909 patients: Criteria found to be 100% sensitive; 100% negative predictive value

1429 pts: 6.5% + CT; 0.4% required neurosurgery

Criteria would have resulted in a 22% decrease in the number of scans ordered

Haydel et al. NEJM 2000; 343:100-105

Head CT In Mild TBI 10% to 20% have a positive CT .2 to 4% have a neurosurgical lesion Patients without LOC or amnesia, normal

exam, and GCS 15 do not need imagingDirect trauma to the temporal areaChildren <3 years

In patients with a GCS of 15, historical and clinical criteria can be used to determine need for CT

Patients with a normal CT can be safely discharged home

Magnetic Resonance Imaging Prospective study 50 TBI patients; CT, MRI, neuropsych 72% had lesions on CT / 80% on MRI MRI identified additional lesions in

52% of patients with lesions on CT No correlation with size of lesions and

length of LOC: inconsistent relationship between lesions and neuropsych findings

Levin et al. J Neurol Neurosurg Psych 1992;55:255

OUT PATIENTS CONDITION* Conscious + good orientation* No neurological deficit* Decreased of complain* No fracture* Social Problems

NOTES :* Seriously complain* Restlessness* Decreased of conscious ( GCS )* Seizures* Lateralization

ICU OBSERVATION

* GCS < 8

* GCS 9 – 15 : with neurological

deficit, cushing respons

* Progresive neurological deficit

* Progresive of complain :

cephalgia , vertigo and vomiting

1. OBSERVATION OF CONSCIOUSNESS

based on GCS

1. Recover

2. SBI

15

151515

15FI15

FI

15FI

2. OBSERVATION OF NEUROLOGICAL DEFICIT

NO LATERALIZATION

Pupil : isocoria

Motoric : normal

LATERALIZATION

Anisocoria

Hemi/Tetra Phareses/Pharalyses

Caused by : Intracranial : Processes Extracranial : Hypoxemia

Bradycardia : Pulse < 60/minute

Hypertension

Cephalgia , Vertigo , Vomiting

CUSHING RESPONSE

OBSERVATION1. GCS 7. Restlessness2. Neurologic Sign 8. Seizures3. Vital Sign : BP, Pulse 9. Urinary4. Position 10. Skin Care5. Fluid 11. ICP Monitoring6. Temperature 12. Drug / Medicine

MANAGEMENT

ABC

Dx

CONSERVATIVE OPERATIVE

SECONDARYSURVEY

PRIMARYSURVEY

MANAGEMENT1. Head positioning○ The tongue drops : losses the muscle

strength○ The head and the body are placed aside

2. A : Airway○ Clearance of respiratory tract

3. B : Breathing○ Massage on the chest○ Oxygenation is given○ Mouth breathing artificial respiration

4. C : Circulation○ Signs : + Pale

+ Decrease of pulse rate

+ Arterial pulse unpalpable

○ Tx : * Stop bleeding

* Infusion

Decerebrate rigidity or abnormal extensor posturing

Decerebrate posturing is also called decerebrate response, decerebrate rigidity, or extensor posturing. It describes the involuntary extension of the upper extremities in response to external stimuli. In decerebrate posturing, the head is arched back, the arms are extended by the sides, and the legs are extended. [6] A hallmark of decerebrate posturing is extended elbows.[12] The arms and legs are extended and rotated internally. [13] The patient is rigid, with the teeth clenched. [13] The signs can be on just one or the other side of the body or on both sides, and it may be just in the arms and may be intermittent. [13]

A person displaying decerebrate posturing in response to pain gets a score of two in the motor section of the Glasgow Coma Scale (for adults) and the Pediatric Glasgow Coma Scale (for infants).Decerebrate posturing indicates brain stem damage, specifically damage below the level of the red nucleus (e.g. mid-collicular lesion). It is exhibited by people with lesions or compression in the midbrain and lesions in the cerebellum.[12] Decerebrate posturing is commonly seen in Pontine strokes which are also known as Locked-In Syndrome. A patient with decorticate posturing may begin to show decerebrate posturing, or may go from one form of posturing to the other. [1] Progression from decorticate posturing to decerebrate posturing is often indicative of uncal (transtentorial) or tonsilar brain herniation. Activation of gamma motor neurons is thought to be important in decerebrate rigidity due to studies in animals showing that dorsal root transection eliminates decerebrate rigidity symptoms. [14]

In competitive contact sports, posturing (typically of the forearms) can occur with an impact to the head and is termed the fencing response. In this case, the temporary posturing display indicates transient disruption of brain neurochemicals, which wanes within seconds.

Decorticate posturing, with elbows, wrists and fingers flexed, and legs extended and rotated inward

Decorticate posturing is also called decorticate response, decorticate rigidity, flexor posturing, or, colloquially, mummy baby.[11] Patients with decorticate posturing present with the arms flexed, or bent inward on the chest, the hands are clenched into fists, and the legs extended and feet turned inward. A person displaying decorticate posturing in response to pain gets a score of three in the motor section of the Glasgow Coma Scale.There are two parts to decorticate posturing.The first is the disinhibition of the red nucleus with facilitation of the rubrospinal tract. The rubrospinal tract facilitates motor neurons in the cervical spinal cord supplying the flexor muscles of the upper extremities. The rubrospinal tract and medullary reticulospinal tract biased flexion outweighs the medial and lateral vestibulospinal and pontine reticulospinal tract biased extension in the upper extremities.The second component of decorticate posturing is the disruption of the lateral corticospinal tract which facilitates motor neurons in the lower spinal cord supplying flexor muscles of the lower extremities. Since the corticospinal tract is interrupted, the pontine reticulospinal and the medial and lateral vestibulospinal biased extension tracts greatly overwhelm the medullary reticulospinal biased flexion tract.The effects on these two tracts (corticospinal and rubrospinal) by lesions above the red nucleus is what leads to the characteristic flexion posturing of the upper extremities and extensor posturing of the lower extremities.Decorticate posturing indicates that there may be damage to areas including the cerebral hemispheres, the internal capsule, and the thalamus.[12] It may also indicate damage to the midbrain. While decorticate posturing is still an ominous sign of severe brain damage, decerebrate posturing is usually indicative of more severe damage as the rubrospinal tract and hence, the red nucleus, is also involved indicating lesion lower in the brainstem.

Opisthotonus in a patient suffering from tetanus. Painting by Sir Charles Bell, 1809.

It is seen in some cases of severe cerebral palsy and traumatic brain injury or as a result of the severe muscular spasms associated with tetanus.Opisthotonus can be produced experimentally in animals by transection of the midbrain (between superior and inferior colliculus) which results in severing all the corticoreticular fibers. Hyperextension occurs due to facilitation of the anterior reticulospinal tract caused by the inactivation of inhibitory corticoreticular fibers which normally act upon the pons reticular formation. It has been shown to occur naturally only in birds and placental mammals.Opisthotonus is more pronounced in infants. Opisthotonus in the neonate may be a symptom of meningitis, tetanus, severe kernicterus, or the rare Maple Syrup Urine Disease. This marked extensor tone can cause infants to "rear backwards" and stiffen out as the mother or nurse attempts to hold or feed them. Opisthotonus can be induced by any attempt at movement such as smiling, feeding, vocalization, or by seizure activity. A similar tonic posturing may be seen in Sandifer syndrome. Individuals with opisthotonus are quite challenging to position, especially in wheelchairs and car seats.Opisthotonus can sometimes be seen in lithium intoxication. It is a rare extrapyramidal side effect of phenothiazines, haloperidol, and metoclopramide.Opisthotonus with the presence of the risus sardonicus is also a symptom of strychnine poisoning.Opisthotonus is also described as a potential CNS symptom of heat stroke along with bizarre behavior, hallucinations, decerebrate rigidity, oculogyric crisis and cerebellar dysfunction.