clinical localization series

1. 23. The Localization of
Lesions Causing Coma
Dr rzgar hamed abdwl

2. The Unresponsive Patient
• Akinetic mutism refers to a state in which the patient, although seemingly awake
remains silent and motionless.
- It can usually be distinguished from psychogenic (often catatonic)
unresponsiveness.
- Signs of frontal release (such as grasp or sucking ) or corticospinal tract damage
favor the diagnosis of akinetic mutism.
- In the catatonic patient, the EEG is normal but in the patient with akinetic
mutism, the EEG may show slow-wave abnormalities
- Lesions that cause akinetic mutism:
>>> affect bilaterally the frontal region (anterior cingulate gyri)
>>> the diencephalo-mesencephalic reticular formation
>>> the globus pallidus, or the hypothalamus
- Metabolic or ictal disorders disrupting the same areas may give rise to a transient
disorder of alertness similar to akinetic mutism

3. • Hyperkinetic mutism with continuous bilateral ballism and dystonia, has been described
in a diabetic with multiple subcortical and cortical infarcts .
• The vegetative state : a chronic neurologic condition characterized by lack of awareness
of self and external stimuli, accompanied by sleep–wake cycles, with preservation of
vital vegetative functions, such as cardiac function, respiration, and maintenance of
blood pressure.
>> Patients in a vegetative state show no evidence of sustained, reproducible, purposeful,
or voluntary behavioral responses to visual, auditory, tactile, or noxious stimuli
>> show no evidence of language comprehension or expression; have bowel and bladder
incontinence; and have variably preserved cranial nerve and spinal reflexes.
>> Present one month after acute traumatic or nontraumatic brain injury
>> Recovery of consciousness from a posttraumatic persistent unresponsive state is
unlikely after 12 months in adults and children
>> Recovery from a nontraumatic after three months is rare in both adults and children.

4. The locked-in syndrome : the patient is mute and motionless (deefferented) but
remains awake, alert, aware of self, and capable of perceiving sensory stimuli.
>> horizontal eye movements are often impaired (the paramedian pontine reticular
formation lesion )
>> vertical eye movements or eyelid movements spared
>> EEG reflects the patient’s state of wakefulness.
>> due to basilar artery thrombosis with ventral pontine infarction, pontine
hemorrhage or tumor, or central pontine myelinolysis
>> These lesions involve the descending motor pathways bilaterally in the basis
pontis but spare the more dorsal reticular formation.
>> Bilateral ventral midbrain lesions ,tentorial herniation , Guillain–Barré syndrome
, or myasthenia gravis may rarely cause this syndrome.

5. Anatomic Substrate of Alertness
• In general, the maintenance of consciousness depends on interaction between
the ascending reticular activating system (ARAS) and the cerebral hemispheres.
• the ARAS lies in the paramedian tegmental region of the posterior portion of
pons and midbrain that extends from the superior half of the pons through the
midbrain to the posterior portion of the hypothalamus and to the thalamic
reticular formation
• when unresponsiveness is caused by brainstem damage, the lesion affects ocular
motility as well.
• Bilateral cerebral hemispheric lesions may cause transient coma
• In the diencephalon, posterior hypothalamic lesions induce prolonged
hypersomnia.
• Acute bilateral damage of the paraventricular thalamic nuclei is attended by
transient unresponsiveness.

6. Signs with Localizing Value in Coma
Respiratory Patterns
1- POST-HYPERVENTILATION APNEA
• reflects mild bilateral hemispheric dysfunction.
• To elicit this phenomenon, the patient is simply asked to take five deep breaths. This maneuver
normally decreases arterial pCO2 by about 10 mm Hg and, in the healthy patient, is followed by
a very brief period of apnea (<10 seconds).
• the post-hyperventilation apnea lasts for as long as 20 or 30 seconds.
2- CHEYNE–STOKES RESPIRATION
• consists of brief periods of hyperpnea alternating regularly with even shorter periods of apnea.
After the apneic phase, the amplitude of respiratory movements increases gradually to a peak
and then slowly wanes to apnea.
• This may follow bilateral widespread cortical lesions , bilateral thalamic dysfunction ,Metabolic
disturbances, such as uremia, diffuse anoxia, and heart failure.

7. 3- HYPERVENTILATION WITH BRAINSTEM INJURY
• Lesions of the midbrain and pons and pulmonary or metabolic causes
• Prolonged and rapid hyperpnea.
• This type of breathing cannot truly be called neurogenic hyperventilation.
• Central neurogenic hyperventilation, responsive to morphine and methadone .
4- APNEUSTIC BREATHING
• characterized by a long inspiratory pause, after which the air is retained for
several seconds and then released.
• lesions of the lateral tegmentum of the lower half of the pons.
5- CLUSTER BREATHING
• Breathing with a cluster of breaths following each other in an irregular sequence
may result from low pontine or high medullary lesions.

8. 6-ATAXIC BREATHING
• has a completely irregular pattern (also called the atrial fibrillation of respiration)
• present in agonal patients, heralds complete respiratory failure and follows
damage of the dorsomedial medulla and severe meningitis
7- ONDINE CURSE
• Pathways from the cerebral cortex subserving voluntary respiration are separate
from those descending from the medulla subserving automatic respiration; thus,
selective impairment of automatic or voluntary breathing is possible .
• Descending pathways that are under voluntary control travel within the dorsal
cord in the region of the corticospinal tract, whereas pathways from primary
medullary respiratory centers travel in the ventrolateral cord, with anatomic
separation of inspiratory and expiratory pathways .

9. • Ondine curse refers to the loss of automatic breathing during sleep.
• This respiratory pattern, obviously absent in comatose patients, is mentioned
here because it occurs with lower brainstem dysfunction.
• Responsible lesions have a similar or somewhat lower location than those that
cause ataxic breathing but are smaller or develop more slowly.
• Both unilateral and bilateral medullary tegmental infarcts have produced this
syndrome.
• This disorder has also been recorded with high cervical cord lesions after surgical
section of the ventrolateral spinal cord for pain relief , probably because of
reticulospinal tract interruption.
Temperature Changes
• Hyperthermia is caused by severe traumatic brain injury
• This is,related to an altered temperature regulation system.
• they correspond to hypothalamic dysfunction and pontine tegmental lesions

12. The Pupils
• The pupillary light reflex is very resistant to metabolic dysfunction. Abnormalities
of this reflex, particularly when unilateral, indicate structural lesions of the
midbrain or oculomotor nerve with A few exceptions are :
1- Atropinic agents instilled into the eyes, applied on the skin, ingested, or given
during cardiopulmonary resuscitation, may cause pharmacologic iridoplegia.
>> In these cases, a solution of 1% pilocarpine applied to the eye will fail to
constrict the pupils, whereas in the case of anoxic pupillary dilation, this
cholinergic agent, acting directly on the constrictor of the iris, produces miosis.
>> Because many patients in coma have small pupils, anticholinergic agents are
sometimes used to facilitate visualization of the optic fundi, thus eliminating a
potentially useful diagnostic indicator.
>> In many cases, a better way to obtain pupillary dilation is by pinching the skin of
the neck (ciliospinal reflex).

13. 2- Glutethimide (Doriden) induces unequal pupils that are midsized or slightly
dilated and poorly responsive to light.
3- Other agents that may cause unreactive pupils include barbiturates (the
pupillary light reflex is more often retained), succinylcholine, and, rarely, other
anticonvulsants, lidocaine, phenothiazines, methanol, and aminoglycoside
antibiotics .
4- Agents other than glutethimide or anticholinergic drugs cause pupillary dilation
only when taken in massive amounts, enough to eliminate respiratory reflexes
5- Hypothermia and acute anoxia may also cause unreactive pupils, which, if
persistent beyond several minutes after an anoxic insult, carry a poor prognosis

14. Various structural lesions causing coma may be associated with pupillary abnormalities :
1. Sleep or bilateral diencephalic dysfunction (metabolic coma) : small pupils that react
well to light (“diencephalic” pupils).
2. Unilateral hypothalamic damage : miosis
and anhidrosis on the side of the body ipsilateral to the lesion.
3. Midbrain lesions :
>> Tectal or pretectal lesions:
- Abolish the light reflex
- the pupils: midsized or slightly large
- may show spontaneous oscillations in size (hippus)
- become larger when the neck is pinched (ciliospinal reflex).
>> Tegmental lesions:
- involve the third nerve nucleus
- pear-shaped pupil or displacement of the pupil to one side (midbrain corectopia) .
- Or midsized and lack light or ciliospinal responses

16. 4. Pontine tegmental lesions:
- small pupils (pinpoint) due to
interruption of descending
sympathetic pathways. 5. Lateral
pontine: ipsilateral Horner syndrome.
6. 3rd compression ( by the uncus of
the temporal lobe) :
- early pupillary dilation
- The light reflex is sluggish or absent,
and, unlike the situation with
midbrain involvement, the pupil
becomes widely dilated owing to
sparing of the sympathetic pathways
(Hutchinson pupil).

17. 7. Other oculomotor nerve lesions:
- causing pupillary abnormalities are less likely to impair consciousness,
except when associated with a subarachnoid hemorrhage.
- Posterior communicating artery aneurysms can compress the third
nerve and a massive subarachnoid hemorrhage may result in coma.
- Rarely, with the Guillain–Barré syndrome patients may become
completely paralyzed and lose even their pupillary response
- With acute neurosurgical lesions, fixed pupils are not necessarily a sign
of irreversible coma (25% of them made a functional recovery)

18. Eye Movements
• In the absence of voluntary eye movements, the assessment of ocular motility in comatose
patients relies heavily on reflex eye movements, including :
- the oculocephalic reflex: elicited by the doll’s eye maneuver
- the oculovestibular reflex: elicited by instillation of cold or warm water into the external
auditory canal .

20. • Because of the absence of cortical control of eye movements, the comatose
patient lacks voluntary saccades, including the quick phase of nystagmus and
tracking eye movements.
• Instead, if the brainstem is intact, the eyelids are closed, and the eyes, slightly
divergent, drift slowly from side to side (roving eye movements).
• Spontaneous blinking requires an intact pontine reticular formation.
>> Blinking induced by a bright light is probably mediated by the superior colliculus
and remains intact despite occipital damage.
>> Absence of blinking only on one side indicates unilateral nuclear, fascicular, or
peripheral facial nerve dysfunction.
>> The eyelids may remain tonically retracted due to failure of levator inhibition in
some cases of pontine infarction (eyes open coma)

23. Some notes apart from the table :
Short-cycle periodic alternating gaze (ping-pong gaze):
• which consists of roving of the eyes from one extreme of horizontal gaze to the
other and back, with each oscillating cycle taking 2.5 to 8 seconds
• indicates :
- bilateral cerebral
- posterior fossa lesion
- basal ganglia infarcts
- Hydrocephalus
- overdose of the monoamine oxidase inhibitor tranylcypromine
• Ping-pong gaze must be differentiated from periodic alternating gaze deviation,
which is an alternating horizontal conjugate gaze deviation lasting 1 to 2 minutes
in each direction, occurs in alert patients with structural lesions involving the
cerebellum and brainstem, such as the ArnoldChiari malformation or
medulloblastoma, but it has been described in obtunded or comatose patients
with hepatic encephalopathy

24. • Ocular bobbing:
- Cold calorics may increase the amplitude and frequency of the bobbing or have
no effect .
- Etiology :
>> intrinsic pontine lesions
>> extra-axial posterior fossa masses (e.g., aneurysm rupture or cerebellar
hemorrhage or infarction)
>> diffuse encephalitis
>> Jakob–Creutzfeldt disease
>> toxic-metabolic encephalopathies (e.g., acute organophosphate poisoning)
• “Typical” ocular bobbing, which is associated with preserved horizontal eye
movements, is thought to be specific but not pathognomonic of acute pontine
injury, whereas “atypical” ocular bobbing, which is associated with absent
horizontal eye movements, is thought to be less helpful in predicting the site of
abnormality

25. • Monocular bobbing (paretic bobbing), which consists of a quick downward
movement of one eye and intorsion or no movement in the other eye, may occur
if there is a coexistent unilateral fascicular oculomotor nerve palsy .
• Disconjugate ocular bobbing, with movements involving sometimes one eye and
sometimes the other, may also occur without oculomotor nerve palsy
• Inverse ocular bobbing (ocular dipping or fast upward ocular bobbing) :
- It Has also been described associated with deafness in a patient with
pinealoblastoma .
- Inverse/reverse ocular bobbing consists of inverse ocular bobbing in which the
eyes do not stop on rapidly returning to primary position but shoot into upgaze
and slowly return to midposition

26. ABNORMALITIES OF LATERAL GAZE
1- Conjugate Gaze:
• When both eyes remain deviated toward the same side in a comatose patient
Lesion sites:
1- the cerebral hemisphere (the frontal eye fields) :
- the eyes “look toward the lesion” (away from the hemiparetic side) but can be brought to the other side with the
oculocephalic maneuver, caloric testing, or both.
- A seizure originating in the frontal or occipital lobes may cause deviation of the eyes and head away from the
lesion
- Thalamic and, rarely, basal ganglionic lesions, almost always hemorrhagic, may produce forced deviation of the
eyes to the side contralateral to the lesion (wrong-way eyes)
2- the pontine tegmentum:
- the eyes look toward the hemiparetic side. Neither the oculocephalic maneuver nor caloric testing overcomes a
pontine gaze palsy.
3- Toxic substances :
- impaired conjugate eye movements, horizontal as well as vertical
- Thiamine deficiency (Wernicke encephalopathy)

27. 2. Disconjugate Gaze
• Isolated failure of ocular adduction, in the
absence of pupillary changes and with
normal vertical eye movements (elicited
by oculocephalic or oculovestibular
reflexes),
• a lesion of the MLF in the upper pons
ipsilateral to the eye that fails to adduct.
• MLF involvement is commonly bilateral in
comatose patients.
• Latent strabismus may become apparent
when the level of alertness is mildly
impaired but disappears in deep coma.

28. Abnormalities of Vertical Gaze
• In patients in light coma, upward gaze can be tested by holding the eyelids open and gently touching
the cornea with a wisp of cotton or a similar object. With this stimulus, the eyeballs tend to roll
upward (Bell’s phenomenon).
• Irrigation of both ears with cold water induces downward deviation of the eyes; warm water induces
upward deviation.
• Disconjugate vertical gaze in the resting position (skew deviation) … brainstem, increased intracranial
pressure, or with hepatic
• Tonic downward deviation of the eyes, often accompanied by convergence, may occur with thalamic
hemorrhage
• Forced downward deviation of the eyes during caloric testing often occurs in coma induced by
sedative drugs
• Tonic upgaze occur in severe anoxic encephalopathy , phenothiazine intoxication.
• Paresis of upward gaze …. bilateral midbrain tectal damage.
• Downward gaze is preferentially affected by bilateral lesions of the superomedial perirubral
Region
• Large midbrain tegmental lesions abolish vertical gaze.
• Bilateral ptosis …massive hemispheric infarction seems to suggest compression of the midbrain

29. Corneal Reflex
• The corneal reflex has a higher threshold in comatose patients.
• decreased corneal sensitivity
• cranial nerve V lesions, ipsilateral lateral pontomedullary lesions, or
contralateral parietal lesions
• impaired eye closure (as with cranial nerve VII lesions and low
pontine lesions).
• the stimulus may induce deviation of the jaw to the opposite side
(corneopterygoid reflex),
• given an intact upper pons and midbrain, the eyes may roll upward (Bell's
phenomenon)

30. • Abnormal extension of the arms with weak flexion of the legs usually indicates damage of the pontine tegmentum
• With even lower lesions involving the medulla, total flaccidity ensues.
• Flaccidity in a critically ill patient can also be produced by a polyneuropathy/ myopathy
• Flexor (“decorticate”) posturing
• Flexion and adduction of arms and wrists with
• extension of lower extremities;
• it suggests hemispheric or thalamic damage, with sparing of
structures below the diencephalons
• Extensor (“decerebrate”) posturing
• adduction, extension,and pronation of the upper extremities
• and extension of the lower extremities;
• It is indicative of injury to the caudal diencephalon, midbrain, or
pons
• Severe metabolic (e.g., anoxic) disorders
Motor Activity of
the Body and Limbs

31. • a metabolic coma (notably hypoglycemic) : may present with the following:
- Hemiparesis
- Decorticate (flexor posturing) and decerebrate (extensor posturing) rigidity
• Lazarus sign refers to complex movements suggesting purposeful activity. In one
instance, the arms, with flexed elbows and hands held together, adopted a
praying position.
• Spinal automatisms may be present in as many as 40% of heart-beating cadavers,
typically within the first 24 hours after total brain destruction,such as facial
movements or a gag reflex, limb or trunk movements are more likely to be
mediated by the spinal cord.

32. Coma-Inducing Lesions Depending on Their Location:
1- Metabolic Encephalopathy (Diffuse Brain Dysfunction)
• The phylogenetically newer brain structures tend to be more sensitive to metabolic injury, like
pallidal necrosis carbon in monoxide poisoning
• Thus, higher cortical functions and attention succumb early to metabolic insults, whereas the
pupillary light reflex remains to the brink of brainstem death.
• By the time decerebrate posturing appears, the corneal reflexes may be severely depressed.
• They may have abnormal movements (tremor, asterixis, myoclonus, and seizures)
• The tremor of metabolic encephalopathy :
- coarse and irregular and ranges from 8 to 10 cycles per second.
- Its amplitude is greatest when the patient holds his hand outstretched, but in less responsive
patients it may be felt by holding the patient’s fingers extended.

33. • Bilateral Asterixis is present with slight stupor and wanes as coma deepens.
• Unilateral asterixis may be seen contralateral to lesions of the mesencephalon,
ventrolateral thalamus, primary motor cortex, or parietal lobe or ipsilateral to
lesions of the pons or medulla
• bilateral asterixis may occur with bilateral lesions of the mid-pons
• Multifocal myoclonus or may be present in uremic and hyperosmolar-
hyperglycemic encephalopathy, carbon dioxide narcosis, and a large dose of
intravenous penicillin

34. • Asymmetric motor findings speak against the diagnosis of metabolic
encephalopathy
• Exceptions:
• downward deviation of the eyes may be occasionally associated with hepatic
encephalopathy
• hemiparesis with hypoglycemia.
• ethylene glycol, produce focal brain injuries with the corresponding
neurologic localizing findings
• Focal seizures are common in metabolic encephalopathies, particularly those
coursing with the breakdown of the blood-brain barrier, such as eclampsia,
malignant hypertension, and acute intermittent porphyria

35. • Generalized myoclonus
• mainly involves the axial musculature, which contracts suddenly, making the patient jump
with a certain periodicity
• It may also appear as irregular brief jerks in both face and limbs.
• The myoclonus is often stimulus sensitive
• is most prominent in the first postresuscitation day and tends to abate spontaneously in
subsequent days.
• The patients often have a burst-suppression pattern on EEGs and cerebral edema or
infarcts on CT scan or MRI.
• Severe anoxic cortical and brainstem damage are the most common pathologic correlates
of generalized myoclonus (also called myoclonic status), which carries a poor prognosis

36. Subtentorial Structural Lesions
• Early in the clinical course, occipital headache, vomiting, and ataxia are usually prominent
• Lesions that compress the upper brainstem
• may cause upward transtentorial herniation of the tectum of the midbrain and of the anterior cerebellar
lobule  giving rise to signs of midbrain dysfunction with coma, - hyperventilation, fixed pupils, and vertical
ophthalmoplegia.
• Lower lesions impinge on the pontine tegmentum
• somnolence,
• pinpoint pupils that react briskly to light,
• oculoparetic nystagmus on lateral gaze,
• truncal ataxia.
• Appendicular ataxia may be so mild as to pass unnoticed.
• As pontine function becomes worse
• horizontal gaze disappears and cannot be elicited with the doll's eye maneuver or caloric testing, whereas
impairment of vertical eye movements clearly lags behind.

37. Supratentorial Structural Lesions
Lateral Herniation

38. lateral extracerebral or temporal lobe masses
push the mesial temporal lobe (uncus anteriorly, parahippocampal gyrus posteriorly) between
the ipsilateral aspect of the midbrain and the free edge of the tentorium
compresses the third cranial nerve and posterior cerebral artery
the ipsilateral pupil becomes progressively dilated and responds sluggishly to light
a hemorrhagic mesial occipital infarct
pushes the midbrain against the rigid edge of the dura on the opposite side of the tentorial opening
carves out a notch (Kernohan's notch) in the lateral aspect of the midbrain, interrupting the cerebral
peduncle (particularly the fibers that project to the leg) on the side opposite the original temporal
lobe lesion
hemiparesis ipsilateral to the original lesion (Kernohan's notch phenomenon)
a false localizing sign
tearing of the paramedian midbrain perforating vessels infarction and hemorrhages (Duret's
hemorrhages)  the sympathetic pathway is damaged in the midbrain  pupil becomes midsize
and unresponsive.
Oculomotor paresis appears first in the eye originally involved and shortly afterward in the other eye.

39. FIG. 23.6. Lateral transtentorial herniation: (A)
basal view, (B) coronal view. In this example, a
subdural hematoma is causing a marked shift
of the midline structures and herniation of the
parahippocampal gyrus through the tentorial
notch. Occlusion of the posterior cerebral
artery, which is pinched between the herniated
hippocampal tissue and the rigid end of the
tentorium, has resulted in medial temporo-
occipital infarction. The midbrain is
compressed against the contralateral free
tentorial edge, causing a laceration of the crus
cerebri (Kernohan notch). Stretching of the
slender perforating branches of the basilar
artery has produced petechial hemorrhages in
the tegmentum of the midbrain (Duret
hemorrhages).

40. Clinical Findings in Uncal Herniation Syndrome

41. • Central Herniation
frontal, parietal, or occipital masses
the supratentorial pressure increases,
first compress the diencephalon
shifts downward and buckles over the midbrain.
Subsequent flattening of the midbrain and pons in the rostrocaudal direction
causes elongation and rupture of the paramedian perforating arteries
infarction and hemorrhages (Duret's) in the tegmentum of the midbrain (first) and pons
(afterward)
Paralleling the pathologic changes of central herniation, the clinical picture reflects an
orderly rostrocaudal progression of brainstem damage.

43. Early Diencephalic Stage
Impaired attention and somnolence

44. Late Diencephalic Stage
• At this stage the patient cannot be aroused.
• Roving eye movements have disappeared,
• tectal dysfunction may result in restriction of upward gaze. Light painful
stimuli fail to elicit any response
• Proper diagnosis and treatment at this stage of the syndrome of central
herniation may still result in recovery of neurologic function. Once the clinical
picture evolves into the next stage (caused by hemorrhages and infarction of
the midbrain tegmentum), the prognosis is very poor, except in children.

46. Midbrain- Upper Pons Stage
• Temperature oscillations are common, and an occasional patient may develop
diabetes insipidus because of stretching of the median eminence of the
hypothalamus.
• The pupils become midsized, unequal, and irregular, often pear-shaped and
eccentric.
• The doll's eye maneuver and caloric testing elicit restricted or no vertical eye
movements.
• The eyes often move disconjugately in both the horizontal and the vertical planes.
• Bilateral impairment of adduction may reflect dysfunction of both third nerve nuclei,
of the medial longitudinal fasciculi, or both.

48. Lower Pontine Stage

49. Medullary Stage
• ataxic breathing soon gives way to apnea.
• The blood pressure drops, and the pulse becomes irregular
• lesions that impinge on the medulla,
• respiratory ataxia evolving to apnea
• circulatory abnormalities precede changes in the level of alertness.
• The medulla is particularly resistant to infarction, spontaneous hemorrhages, and even traumatic
lesions.
• However, it is preferentially affected in Listeria monocytogenes rhombencephalitis and in Leigh's
disease

50. False localizing signs :
- the Sixth nerve palsy and papilledema
- Ophthalmoplegias
- trigeminal neuralgia or numbness
- unilateral or bilateral deafness
- facial palsy
- weakness in the distribution of the ninth to twelfth cranial nerves may appear as
a consequence of raised intracranial pressure with a supratentorial lesion.

51. Subtentorial Structural Lesions
• Early in the clinical course, occipital headache, vomiting, and ataxia are usually prominent
• Lesions that compress the upper brainstem
• may cause upward transtentorial herniation of the tectum of the midbrain and of the anterior cerebellar
lobule  giving rise to signs of midbrain dysfunction with coma, - hyperventilation, fixed pupils, and
vertical ophthalmoplegia.
• Lower lesions impinge on the pontine tegmentum
– somnolence,
– pinpoint pupils that react briskly to light,
– oculoparetic nystagmus on lateral gaze,
– truncal ataxia.
– Appendicular ataxia may be so mild as to pass unnoticed.
• As pontine function becomes worse
– horizontal gaze disappears and cannot be elicited with the doll's eye maneuver or caloric testing,
whereas impairment of vertical eye movements clearly lags behind.

52. • lesions that impinge on the medulla,
• respiratory ataxia evolving to apnea
• circulatory abnormalities precede changes in the level of alertness.
• The medulla is particularly resistant to infarction, spontaneous hemorrhages,
and even traumatic lesions.
• However, it is preferentially affected in Listeria monocytogenes
rhombencephalitis and in Leigh's disease

53. Psychogenic Unresponsiveness
• The patient may hold the eyes forcibly closed and resist eyelid opening
• or may keep the eyes open in a fixed stare, interrupted by quick blinks.
• The pupils, which are of normal size and position, react to light unless a cycloplegic drug has
been instilled into them.
• The doll's eye maneuver elicits random or no eye movements.
• Caloric testing is more helpful because it gives rise to classic vestibular nystagmus with a
quick component that requires activity of the frontal eye fields. This quick component is,
conversely, absent in comatose patients.
• Muscle tone and reflexes are normal.
• The patient may hyperventilate or breathe normally.
• Psychogenic unresponsiveness often recurs and as such is frequently misdiagnosed as an
epileptic or migranous disorder.

54. GCS

55. Diagnosis of Death Caused by Brain Destruction
• Criteria for the diagnosis of death caused by brain destruction in adults
recommends the following steps:
I. The clinical evaluation (prerequisites)
A. Establish irreversible and proximate cause of coma.
B. Achieve normal core temperature.
C. Achieve normal systolic blood pressure: Neurologic examination is usually
reliable with a systolic blood pressure of >100 mm Hg.
D. Perform one neurologic examination

56. II. The clinical evaluation (neurologic assessment).
A. Noxious stimuli should not produce a motor response other than spinally
mediated reflexes.
B. Absence of brainstem reflexes.
a. Absence of pupillary response to a bright light is documented in both eyes.
- Usually the pupils are fixed in a midsize or dilated position (4–9 mm).
- Constricted pupils suggest the possibility of drug intoxication.
b. Absence of ocular movements using oculocephalic testing and oculovestibular
reflex testing: Movement of the eyes should be absent during 1 minute of
observation. Both sides are tested, with an interval of several minutes
c. Absence of corneal reflex
d. Absence of facial muscle movement to a noxious stimulus.
e. Absence of the pharyngeal and tracheal reflexes.

57. C.Apnea.
a. Absence of a breathing drive is tested with a CO2 challenge. Documentation of
an increase in PaCO2 above normal levels is typical practice.
It requires preparation before the test.
b. Prerequisites:
(i) normotension
(ii) Normothermia
(iii) Euvolemia
(iv) Eucapnia (PaCO2 35–45 mm Hg)
(v) the absence of hypoxia
(vi) no prior evidence of CO2 retention (i.e., chronic obstructive pulmonary
disease, severe obesity).

58. c. Procedure:
1. Adjust vasopressors to a systolic blood pressure >100 mm Hg.
2. Preoxygenate for at least 10 minutes with 100% oxygen to a PaO2 > 200 mm Hg.
3. Reduce ventilation frequency to 10 breaths per minute to eucapnia.
4. Reduce positive end-expiratory pressure (PEEP) to 5 cm H2O
5. If pulse oximetry oxygen saturation remains >95%, obtain a baseline blood gas
(PaO2, PaCO2, pH, bicarbonate, base excess).
6. Disconnect the patient from the ventilator.
7. Preserve oxygenation (e.g., place an insufflations catheter through the
endotracheal tube to a point near the level of the carina and deliver 100% O2 at 6
L/min).
8. Look closely for respiratory movements for 8 to 10 minutes. Respiration is
defined as abdominal or chest excursions and may include a brief gasp.

59. 9. Abort if systolic blood pressure decreases to <90 mm Hg.
10. Abort if oxygen saturation measured by pulse oximetry is <85% for >30
seconds. Retry procedure with T piece, CPAP 10 cm H2O, and 100% O2 12 L/min.
11. If no respiratory drive is observed, repeat blood gas after approximately 8
minutes.
12. If respiratory movements are absent and arterial PCO2 is > 60 mm Hg (or 20
mm Hg increase in arterial PCO2 over a baseline normal arterial PCO2), the apnea
test result is positive (i.e., supports the clinical diagnosis of death).
13. If the test is inconclusive but the patient is hemodynamically stable during the
procedure, it may be repeated for a longer period of time (10–15 minutes) after
the patient is again adequately preoxygenated.
(( In some cases, ancillary tests, such as electroencephalography or neuroimaging,
are needed))