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2.10 · Dementia

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5 New variant CJD (vCJD) : this form is related to

consumption of meat infected with BSE.It is generally seen in younger patients than the classical CJD.

sCJD is characterized by rapidly progressing dementia, with 50 % chance of death within 5 months of symptom onset. It is typically seen in patients 60–75 years old. Other neurological features include cerebellar ataxia, pyramidal and extrapyramidal signs, and cortical blindness. Death in sCJD patients is most commonly due to pneumonia.

vCJD is linked to consumption of infected cattle meat with BSE. vCJD is seen in younger age than sCJD, and the neurological symptoms are nonspeci c, with patients o en showing psychiatric and behavioral changes. Incubation period of the disease is approximately 10 years. MRI plays an important role in establishing the diagnosis, since de nite diagnosis of prion diseases requires pathological sample examination.

Signs on MRI

5 In sCJD, the brain shows hyperintense signal

changes in the caudate head and the putamen on T2W images (. Fig. 2.10.9 ). This sign can be observed in other diseases like carbon monoxide poisoning, hypoglycemia, hemolytic uremic syndrome, and Wilson’s disease.

5 In vCJD, there are bilateral, almost symmetrical T2

hyperintense lesions found in the pulvinar, the

most posterior thalamic nucleus ( positive pulvinar sign ) (. Fig. 2.10.10 ). Normally, the pulvinar is the most hypointense nuclei of the deep gray matter on T2W images. Positive pulvinar sign is a highly sensitive sign of vCJD (. Fig. 2.10.10 ) .

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. Fig. 2.10.9 Axial FLAIR brain MR illustration demonstrates

the MR signs of sCJD

. Fig. 2.10.10 Axial FLAIR brain MR illustration demonstrates

the bilateral posterior thalamic (pulvinar) hyperintense lesions in vCJD (positive pulvinar sign)

Further Reading

Becker T, etal. MRI white matter hyperintensity in neurolep-

tic malignant syndrome (NMS)- a clue to pathogenesis? J Neural Transm Gen Sect. 1992;90:151–9.

Deleu D, etal. Downbeat nystagmus following classical heat

stroke. Clin Neurol Neurosurg. 2005b;108:102–4.

Manto M, etal. Cerebellar gait ataxia following neuroleptic

malignant syndrome. J Neurol. 1996;243:101–6.

McLaughlin CT, etal. MR imaging of heat stroke: external

capsule and thalamic T1 shortening and cerebellar injury. AJNR Am J Neuroradiol. 2003;24:1372–5.

Yaqub BA, etal. Pancerebellar syndrome in heat stroke: clini-

cal course and CT scan  ndings. Neuroradiology. 1987;29:294–6.

2.13 Aphasia

Aphasia is a term used to describe the inability to use language. Brodmann has divided the brain into areas according to the cerebral functions. Language is controlled by two main areas: Broca’s and Wernicke’s areas. Broca’s area (area 45)

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Chapter 2 · Neurology

occupies the opercular and triangular parts of the inferior frontal gyrus. In contrast, Wernicke’s area (areas 21 and 42) occupies the posterior part of the superior temporal gyrus.

Neural Control of Speech

1 . Occipital lobe : the occipital lobe (Brodmann’s areas 17,

18, and 19) receives visual information during reading ( word shapes ) and projects them to di erent brain regions specialized with language processing.

2 . Angular gyrus : the dominant angular gyrus (usually the

le ) receives inputs from the occipital, temporal, and parietal lobes, and it associates words with the their objects and their meaning .

3 . Wer nicke’s area : Wernicke’s area (Brodmann’s areas 21

and 42) is the auditory association area responsible for assembling words into sentences . Wernicke’s area is a region that involves part of the supramarginal gyrus, the angular gyrus, the bases of the middle gyrus, the posterior part of the superior temporal gyrus, and the planum temporale.  e planum temporale is the superior aspect of the temporal lobe, and it lies in the depth of the Sylvian  ssure.

4 . Arcuate fasciculus (Wernicke’s arc) : arcuate fasciculus is

an axonal band that transfers information from Wernicke’s area (temporal lobe) to Broca’s area (frontal lobe).  e arcuate fasciculus lies within the superior longitudinal fasciculus in the dominant hemisphere (usually the le ).

5 . Broca’s area : Broca’s area (Brodmann’s area 45) occupies

the opercular and triangular parts of the le inferior frontal gyrus, and it is the “primary language area” responsible for words motor articulation planning .

6 . Motor cortex : the motor cortex speech (precentral

gyrus, Brodmann’s area 4) receives inputs from Broca’s area regarding spoken sentences to be produced, and it is responsible for motor articulation of spoken words/ sentences .

7 . Lips : the lip is important for the  nal sound

manipulation.  e lower lip is much faster and stronger than the upper one.

8 . To n g ue : tongue movement against the hard palate

causes the production of the majority of phonemes in English.

9 . Velum/velopharyngeal opening : for nonnasal speech, the

velum closes the gap between it and the nasopharynx (nasopharyngeal opening) during speech by the action of the levator veli palatini muscle .

10. Mandible : the mandible movement assists in tongue movement.  e mandibular elevators are temporalis, masseter, and medial pterygoid muscles, and the mandibular depressors are digastric , mylohyoid , geniohyoid , and lateral pterygoid muscles .

11. Hyoid bone : the hyoid bone is attached to the larynx,

which will cause change in the position of the larynx/ SVT during speaking by the action of attaching

muscles, causing di erent voice resonance.  e hyoid moves during mandibular depression.

12. Supralaryngeal vocal tract (SVT) : the SVT acts in a

manner similar to the tube of a woodwind instrument,  ltering the source of acoustic energy emitted from the vocal cords as series of air pu s.  e SVT’s di erent cross-sectional areas cause resonance of the sound.

13. Vocal cords : the vocal cords vibrate rapidly moving

inward and outward during phonation, converting the steady  ow of air  owing from the lungs through the trachea into a series of cyclic “pu s” of air that becomes sounds. When vocal cords close, their vibration results in voiced sounds; when they open, this vibration stops, and unvoiced sounds result.

14. Lung : speech occurs during expiration, where the

outward  ow of air from the lungs usually provides the power of speech production.

Aphasia Pathophysiology and Subtypes

Language production is a very complex mechanism that can be oversimpli ed by the following models: visual information reaches the occipital lobe ( Brodmann’s area 17 , 18 , and 19 ) and processed in various ways, and then the information are projected via the dominant angular gyrus , which associ- ates words with the object and its attributes; the words are then transferred to Wernicke’s area , which assemble them into sentences; Wernicke’s area then activates the appropriate motor programs in Broca’s area , most likely via the superior longitudinal fasciculus . Activation of the word’s motor program in Broca’s area activates the motor cortex ( precentral gyrus , area 4 ). Aphasia can result in disturbance of this neural loop, manifested as: 1 . Broca’s aphasia results in defect in the motor activation of

words.  e patient tries to produce words, but he is unable to or produces few written or spoken words. However, they may speak or write in a telegraphic way ( only the most meaningful words in a sentence are produced ). Broca’s aphasia deprives the motor cortex from the instruction needed to generate language. Broca’s aphasia is also known as expressive aphasia . On CT and MRI , Broca’s aphasia is detected when the clinical picture shows expressive aphasia with a brain lesion that a ects the opercular and triangular parts of the le inferior frontal gyrus (

2 . Wernicke’s aphasia results from the inability to assemble

sentences. Patients with Wernicke’s aphasia are able to produce spoken or written words, but the words or their sequence in a sentence is defective in their linguistic content ( sometimes called cocktail hour speech ).  e patient may substitute one letter or a word for another (paraphasia), insert new meaningless words ( neologism ), or string words together in order to convey little or no meaning ( jargon aphasia ). Wernicke’s aphasia is also known as receptive aphasia . On CT and MRI , Wernicke’s aphasia is detected when the clinical picture shows receptive aphasia with a brain lesion that a ects the

. Fig. 2.13.1 ).

2.13 · Aphasia

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. Fig. 2.13.1 Multiple brain CT postcontrast, axial ( a , b ), and coronal ( c , d ) images of a patient presented with aphasia; the CT shows left cerebral

infarction that aﬀ ects the frontotemporal area, including the Broca’s area ( arrows ). The linear contrast enhancement seen in the images is due to inﬂ ammatory hyperemia of acute stroke (luxury perfusion)

le -sided supramarginal gyrus, the angular gyrus, the bases of the middle gyrus, the posterior part of the superior temporal gyrus, and/or the planum temporale (. Fig. 2.13.2 ).

3 . Conduction (associative) aphasia : it is a rare form of

aphasia due to damage to the superior arcuate fasciculus, the  bers associating Wernicke’s area to Broca’s area.  e superior arcuate fasciculus lies below the supramarginal gyrus in the temporal lobe. Patients with conduction aphasia are unable to repeat sentences, words, or phrases (hallmark of this condition). Patient’s ability to repeat numbers is typically much better than their ability to

repeat words. Patients also may have di culty in  nding a word to describe a person or an object. On MRI , conduction aphasia can be detected via MR tractography (di usion tensor imaging), which typically shows lesion a ecting the superior longitudinal fasciculus.

4 . Anomic (nominal) aphasia : it is an inability to name

objects, and patients classically know the object or the person’s name, but they have di culty in  nding their names. Unlike Wernicke’s aphasia, paraphasias are rare. Anomic aphasia usually arises due to destruction of the angular gyrus in the dominant hemisphere (le hemisphere). Speech and comprehension are not

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. Fig. 2.13.2 Axial CT ( a ), axial T2W MR image ( b ), axial DW-MR image, ( c ) and coronal FLAIR-T2-MR image ( d ) of a patient with Wernicke’s aphasia

showing ischemic cerebral insult that involves the left-sided superior and middle temporal gyri ( arrows )

a ected. On MRI , a lesion (e.g., infarction) is seen a ecting mainly the le angular gyrus.

5 . Global aphasia : this type of aphasia results from a

widespread damage of the language center of the le

hemisphere due to anterior and posterior lesions a ecting both Broca’s and Wernicke’s areas together. Typically, global aphasia can arise due to occlusion of the proximal portion of the middle cerebral artery. Patients

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su er from symptoms of both Broca’s and Wernicke’s aphasias combined. On CT and MRI , global aphasia imaging typically shows extensive damage to the le (dominant) hemisphere involving both Broca’s and Wernicke’s regions.

6 . Transcortical sensory aphasia : it is a very rare form of

aphasia that arises when Broca’s area, Wernicke’s area, and the arcuate fasciculus are undamaged but are cut from the rest of the brain, usually a er watershed infarction.  e infarcted areas usually are a ecting Brodmann’s areas 37, 22, and 39. Patients are characterized by well-preserved memory and repetition abilities but are unable to read or write. On MRI , transcortical sensory aphasia classically is associated with watershed infarction a ecting Brodmann’s areas 37, 22, and 39.

7 . Subcortical aphasia : this aphasia arises due to lesions

involving the anterior subcortical area involving the internal capsule and putamen.  e lesion a ects the language  ber output impairing articulation. On CT and MRI , a lesion is seen a ecting the internal capsule with clinical presentation of aphasia (

8 . Primary progressive aphasia : it is a part of frontotemporal

degeneration (Pick’s disease), which is characterized by deterioration of language for at least 2 years before the onset of cognitive de cits. In its early stages, PPA is o en mistaken for Alzheimer’s disease, because patients are

. Fig. 2.13.3 ).

o en presenting with language (naming) impairment. On MRI , primary progressive aphasia shows signs of frontotemporal degeneration and asymmetrical le perisylvian region pathology or atrophy.

9 . Akinetic mutism : it is a rare condition that arises due to

acute thalamic lesion, which can be confused with global aphasia. In contrast to global aphasia, akinetic mutism arises due to lesions of the dorsomedial and ventromedial thalamus and usually develops in the acute period of thalamic hemorrhage and tends to show improvement.

D i ﬀ erential Diagnoses and Related Diseases

Landau–Kle ner syndrome (acquired epileptic aphasia) is a rare syndrome characterized by an acquired receptive and expressive aphasia with epileptic seizures in a previously normal child.  e disease is diagnosed based on speci c clinical and electroencephalography (EEG) criteria. Children with Landau–Kle ner syndrome (LKS) classically present between 3 and 8 years (>50 % of cases) with deafness, behavioral disturbance (>75 % of cases), and loss of auditory verbal understanding ( agnosia ) of speech. EEG classically shows bitemporal, multifocal, or generalized, high-amplitude spikes and wave discharges.  e EEG may be normal in the evolutionary stages of the condition and almost always apparent during nonrapid eye movement (REM) sleep.  erefore, children suspected with LKS should have EEG during sleep, especially if the record during awake is normal.  e disease cause is unknown; however, cases of LKS have been reported in patients with focal subacute encephalitis, neurocysticercosis, and cerebral arteritis. MRI may show signs of white matter demyelinating lesions a ecting the frontal lobe or the centrum semiovale.

. Fig. 2.13.3 Plain brain CT image of a patient presented with aphasia;

the CT showed hemorrhagic infarction of the striate arteries that involves the left internal capsule region ( arrowhead ); the CT diagnosis suggests subcortical aphasia, in conjunction with the clinical presentation

Selected Readings

Barbas H, etal. Frontal-thalamic circuit associated with lan-

guage. Brain Lang. 2013;126:49–61.

Borovsky A, etal. Lesion correlates of conversational speech

production de cits. Neuropsychologia. 2007;45:2525–33.

George A, etal. Primary progressive aphasia: a comparative

study of progressive non uent aphasia and semantic dementia. Neurol India. 2005;53(2):162–6.

Guenther FH, etal. A neural theory of speech acquisition

and production. J Neurolinguistics. 2012;25:408–22.

Honda M. Human speech production mechanisms. NTT

Technical Review. 2003;1(2):24–9.

Lee A, etal.  e contribution of neuroimaging to the study of

language and aphasia. Neuropsychol Rev. 2006;16:171–83.

Lieberman P, etal.  e anatomy, physiology, acoustics and

perception of speech: essential elements in analysis of the evolution of human speech. J Hum Evol. 1992;23:447–67.

Ozeren A, etal. Global aphasia due to le thalamic hemor-

rhage. Neurol India. 2006;54(4):415–7.

Perniola T, etal. A case of Landau-Kle ner syndrome sec-

ondary to in ammatory demyelinating disease. Epilepsia. 1993;39(2):551–6.

Salamon N, etal.  e human cerebral cortex on MRI: value

of coronal plane. Surg Radiol Anat. 2005;27:431–43.

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2.14 Squint (Strabismus)

Strabismus , also known as squint , is de ned as deviation of an

eye’s visual axis from its normal position (ocular malalignment).  e typical clinical manifestation of strabismus is double vision (diplopia). Diplopia is a term used to describe double vision, and it occurs when the two eyes are not misaligned in straight ahead gaze or during movement. It can arise due to squint or due to a disease a ecting the motor nerves (e.g., palsies ) or the ocular muscles (e.g., Grave’s dis- ease ).

Neural Control of Ocular Muscles

1 . Oculomotor nerve (CN 3) : its nucleus is located in the

midbrain and supplies all of the extraocular muscles except the superior oblique muscle and the lateral rectus muscle .

2 . Trochlear nerve (CN 4) : its nucleus is located in the

midbrain and supplies the superior oblique muscle .

3 . Abducens nerve (CN 6) : its nucleus is located in the pons

and supplies the lateral rectus muscle .

4 .  e medial longitudinal fasciculus (MLF) : it controls

vertical eye movement (. Fig. 2.14.1 ). Lesions to the MLF cause vertical gaze palsy ( Parinaud’s syndrome ).

5 . Paramedian pontine reticular formation (PPRF) : it

controls horizontal eye movement.

2 . Paralytic strabismus : it results from paralysis of one or

more eye muscles.  is form di ers from concomitant strabismus in that the angle of deviation does not remain constant in every direction of gaze. Concomitant strabismus usually occurs in children , whereas paralytic strabismus primarily a ects adults.

Risk factors for strabismus include family history, low birth weight, maternal cigarette smoking, increasing maternal age, retinopathy of prematurity, and refractive errors. Strabismus is described as: 1 . Esotropia : the eye is inverted inward . Esotropia compro-

mises up to 60 % of all types of strabismus in the West, with up to 90 % of cases occurring before 5 years of age. Esotropia has to be corrected before the age of 7 years since the risk of amblyopia ( the brain shuts down the devi- ated eye ) is high.

2 . Exotropia : the eye is inverted outward . Exotropia is less

commonly seen compared with esotropia, and it is common among Asian population.  e disease tends to a ect older children than those a ected by esotropia, and the risk of amblyopia is lower than esotropia generally.

3 . Hypertropia : the eye is inverted upward . Hypertropia is

not common compared to eso- and exotropias, with up to 30 % of cases are associated with the fourth cranial nerve palsy . Other causes of hypertropia include Brown’s syndrome and primary inferior oblique overaction.

4 . Hypotropia : the eye is inverted downward.

Pathophysiology

 ere are two major types of manifest strabismus: 1 . Concomitant strabismus (from the Latin comitare ,

accompany): the deviating eye accompanies the leading eye in every direction of movement.  e angle of deviation remains the same in all directions of gaze.

. Fig. 2.14.1 Axial T1W MR illustration demonstrates the normal

location of the medial longitudinal fasciculus on MRI (yellow nuclei)

Related Disorders

1 . Amblyopia : the brain responds to the childhood

strabismus by suppressing the image from the deviating eye to prevent the diplopia, resulting in amblyopia (lazy eye). Amblyopia is not corrected by glasses, and if not treated before the age of 7, the visual loss is irreversible. When strabismus develops in an adult (>7years of age), it results in double vision ( diplopia ), and it usually arises due to cranial nerve injuries a ecting the third, fourth, and sixth cranial nerves, ocular muscle disease (e.g., Brown’s syndrome ), or neuromuscular junction disorder a ecting the ocular muscles (e.g., myasthenia gravis ).

2 . Heavy eye syndrome : heavy eye phenomenon presents as

progressive esotropia and hypotropia in high myopia. It appears to be due to compression of the lateral rectus muscle against the lateral orbital wall by the enlarged myopic globe or due to degeneration of the lateral rectus–superior rectus (LR–SR) band, which joins the lateral and superior rectus muscles. Patients present with acute or subacute strabismus with esotropia that can be misdiagnosed as stroke or mass lesion in the brain.

3 . Congenital  brosis of the extraocular muscles (CFEOM)

syndrome : it is an autosomal recessive disease present since early infancy characterized by strabismus and congenital nonprogressive restrictive ophthalmoplegia

2.14 · Squint (Strabismus)

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123

with or without ptosis.  e disease is divided into CFEOM1, CFEOM2, CFEOM3, and Tukel syndrome. CFEOM is caused by mutation of the FEOM1 gene located on chromosome 12p11.2-q12.  e main pathological cause of CFEOM is hypoplasia of the superior division of cranial nerve 3 (oculomotor nerve, CN III) branches with maldirection of its  bers.

Signs on MRI

1. The role of MRI in squint is to exclude cerebral lesions

(. Fig. 2.14.2 ) and to evaluate the ocular muscles, typically via oculodynamic MRI. Oculodynamic MRI is a technique that uses cine MR images to evaluate the eye movement in motion. Typically, T2W images are taken in axial images, and the patient is asked to look to the right and left while the MR is scanning in cine sequence to evaluate the medial and lateral rectus muscles (. Fig. 2.14.3 ). For the superior and inferior rectus

Congenital  brosis syndrome may be seen in association with Joubert’s syndrome and Marcus Gunn jaw-winking phenomenon. Patients with CFEOM show bilateral severe limitation in vertical gaze with their eyes partially or completely  xed in a strabismic and hypotrophic position due to extraocular muscles  brosis.  e horizontal gaze is normal.

muscles, the same technique is used with sagittal images that are taken for each eye.

2 . Heavy eye syndrome : on MRI (1) the lateral

rectus–superior rectus (LR–SR) band is deﬁ cient or degenerated causing the lateral rectus muscle to be displaced inferiorly from the globe center. The lateral rectus muscle can be displaced in elderly people between 2 and 4 mm, but in heavy eye syndrome, the lateral rectus is displaced 4.5–6.1 mm from the globe center; (2) the inferior rectus muscle in the aﬀ ected eye

. Fig. 2.14.2 Axial ( a , b ) and coronal ( c ) T2W images of a 2-year-old patient with Coxsackievirus encephalitis presented with strabismus.

The inﬂ ammatory changes involve the midbrain nucleus bilaterally ( arrowheads )

. Fig. 2.14.3 Sequential, axial, T2W, oculodynamic cine MR images of a 41-year-old patient presented with left-sided third cranial nerve

palsy. On the dynamic imaging, the left eye ( arrows ) is seen ﬁ xed laterally by the action of an intact lateral rectus and paralyzed medial rectus muscle. The right eye, in contrast, is normally moving when the patient moves the right eye from the left side ( a ) into the right side ( c ) passing through the middle ( b ), when the patient is asked to move his eyes from right to left ( arrowheads ). The left eye remained paralyzed in all images from ( a ) to ( c )

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(Brodmann’s area 5) and is responsible for voluntary

can show displacement; and (3) the aﬀ ected eye can show elongation (myopia) with compression over the

lateral rectus muscle.

3 . CFEOM : on MRI, there is agenesis of the corpus

callosum, basal ganglia, and cerebellar atrophies, and hypoplasia of the oculomotor nerve may be seen in association with CFEOM syndrome; on T1W coronal orbital images, CFEMO shows high T1 signal intensity on T1W images with small volume ocular muscles. Also, selective involvement and atrophy of the superior rectus–levator muscles are characteristic signs observed in CFEMO.

turning both eyes horizontally .

2 . Higher centers : higher centers that contribute to the eye

movement include the anterior cingulated gyrus and parietotemporal cortex (including the insula and hippocampus).

3 .  alamus : a lesion to the posterolateral thalamus can

initiate nystagmus.

4 . Midbrain : apart from holding the oculomotor (CN 3)

and trochlear (CN 4) nuclei, the midbrain participates in eye movement via the interstitial nucleus of Cajal

. Fig. 2.15.1 ) and the rostral interstitial nuclei of the

( medial longitudinal fasciculus ( riMLF ), both of which are involved in the control of vertical and torsional gaze.

5 . Oculomotor nerve (CN 3– midbrain) : it supplies all the

References

Demer JL, etal. High-resolution magnetic resonance imag-

ing demonstrate abnormalities of motor nerves and extraocular muscles in patients with neuropathic strabismus. J AAPOS. 2006;10:135–42.

Durnian JM, etal. Treatment of “heavy eye syndrome” using

simple loop myopexy. J AAPOS. 2010;14:39–41.

Hickman SJ. Neuro-ophthalmology. Pract Neurol.

2011;11:191–200.

Rutar T, etal. “Heavy Eye” syndrome in the absence of high

myopia: a connective tissue degeneration in elderly strabismic patients. J AAPOS. 2009;13:36–44.

Yoshida K, etal. Congenital  brosis of the extraocular mus-

cles (CFEOM) syndrome associated with progressive cerebellar ataxia. Am J Med Genet A. 2007;134A:1494–501.

ocular muscles except the lateral rectus muscle and the

superior oblique muscle .  e oculomotor nucleus receives

a erent  bers from the riMLF and the interstitial nucleus

of Cajal . 6 . Trochlear nerve (CN 4– midbrain) : it supplies the

superior oblique muscle , and its nucleus is located on top of the medial longitudinal fasciculus .

7 . Abducens nerve (CN 6– pons) : it supplies the lateral

rectus muscle , and it receives inputs from the vestibulocochlear nerve (CN 8) regarding the semicircular canal position in space via the paramedian pontine reticular formation (PPRF) .  e abducens nucleus sends axons to the medial rectus muscle via axons that cross and ascend to the oculomotor nucleus (CN 3) via the medial longitudinal fasciculus (

. Fig. 2.15.2 ).  e end

result is the movement of the medial rectus in the same

2.15 Nystagmus

 e function of the ocular motor system is to hold images stable on the fovea. Nystagmus is de ned as the inability to

direction of the lateral rectus muscle during eye movement. Only neurons that innervate the medial rectus muscle in the oculomotor nucleus receive this ascending, crossed input from the abducens nucleus

maintain stable foveal vision, resulting in involuntary oscillation of the eyes ( seeing illusionary movement in the visual  eld ). It may be congenital or acquired in onset. Congenital nystagmus will present within the  rst 6 months a er birth.

Congenital nystagmus has two main causes of origin:

sensory and motor. Sensory nystagmus results from a erent pathway disease of the globes, optic nerves, optic chiasm, or optic tracts in children who lose their vision before 4–6 months of age. A child who sustains bilateral loss of vision a er the age of 6 months will not develop sensory nystagmus. Motor nystagmus , in contrast to sensory nystagmus, results from an anomaly of the central oculomotor control system. It usually presents within weeks a er birth. It is typically binocular and conjugate and is associated with nearly normal visual acuity.

Neural Control of Eye Movement

1 . Frontal eye  eld (Brodmann’s area 8) : this is a cerebral

cortical region that lies anterior to the premotor cortex

. Fig. 2.15.1 Axial T1W MR illustration demonstrates the normal

location of the interstitial nucleus of Cajal on MRI (yellow nuclei)

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