Basilar Artery Thrombosis LESIONS OF MIDBRAIN LOCKED-IN SYNDROME Basilar Artery Thrombosis Basilar artery supplies most of the brainstem, thus occlusion is commonly catastrophic resulting in quadriplegia and multiple cranial nerve deficits. Death from respiratory failure is common. The term locked-in syndrome has been used to described quadriplegia and a mute but alert state in patients with pathologic lesions in the ventral pons. Because of the bilateral involvement of the corticospinal and remaining corticobulbar tracts, the patient is unable to move or speak, although remaining conscious. The only movements that remain by which the patient can communicate is blinking of the eyelids and vertical movements of the eyes. LOCKED-IN SYNDROME with complete basilar artery thrombosis

LESIONS OF PONS The arterial territories of the pons are divided into 4 zones: large anteromedial, smaller anterolateral, large lateral and a small dorsal arterial zone. ANTEROMEDIAL: structures include the medial pontine nuclei and pontocerebellar fibers, medial portion of the corticospinal tracts, fibers of the VII nerve medial wedge of VI nerve nuclei and emerging VI nerve fascicles, paramedian pontiine reticular formation PPRF-horizontal gaze palsy center. And MLF. ANTEROLATERAL: structures include the lateral pontine nuclei and pontocerebellar fibers, lateral portion of the corticospinal tracts. The anterolateral zone donot extend l;aterally to involve the spinothalamic tracts. Fig. Brain stem stroke: Axial DWI &ADC images show bright and dark signal respectively on the left side of the brain stem. Findings compatible with acute stroke. MRA shows irregularity of the basilar artery due to atherosclerosis.

LESIONS OF PONS LATERAL: structures are different at upper and lower pons. In the lower it includes lateral pontione nuclei, pontocerebellar fibers inferior and middle cerebellar peduncle, medial lemnisci and lateral spinothalamic tract and lateral lemnisci, VII nerve nuclei and fasciscles, V nerve complex, the VIII nerve complex, most of the VI nerve nuclei DORSAL: this zone is present only in the upper pons and not in the lower. Dorsal pontine structures include lateral lemnisci posrtion of superior cerebellar peduncle, the loci cerulei and mesencephalic nuclei of V nerve.

MILLARD-GUBLER SYNDROME LESIONS OF PONS MILLARD-GUBLER SYNDROME Ipsilateral facial palsy and contralateral hemiplegia MG syndrome is characterized by ipsilateral facial palsy, due to involvement of the root fibers and contralateral hemiplegia from involvement of corticospinal fibers. Most of the patients with this syndrome show some other associated neurological abnormalities because of involvement of the associated cranial nerve nuclei.

Lower dorsal pontine syndrome LESIONS OF PONS FOVILLE'S SYNDROME Lower dorsal pontine syndrome This syndrome may result from lesions to the dorsal tegmentum of the lower pons. The patient exhibits ipsilateral lower motor neuron paresis of the whole face (nucleus & fibers of CN VII), horizontal gaze palsy on the ipsilateral side (CN VI nucleus), and contralateral hemiplegia (corticospinal tract) with sparing of the face.

LESIONS OF THE MEDULLA The anterior or ventral portion of the medulla contains the pyramids; thus, lesions involving this area of the medulla could result in contralateral weakness or paralysis of the extremities. The face is not involved. However, since the hypoglossal nerve (XII) exits from the ventrolateral sulcus, just lateral to the pyramidal tracts, lesions in this area often affect this nerve, resulting in ipsilateral weakness and atrophy of the tongue. If the lesion extends dorsally, it also will impact on the medial lemniscus, thus producing deficits of position sense, stereognosis, and vibratory perception in the contralateral extremities, while pain and temperature may be preserved. Inferior olivary nucleus XII nerve Nuclei Nuclei XII nerve Nucleus Ambiguus Spinal nucleus of V nerve Nucleus Ambiguus Spinal nucleus of V nerve X nerve Solitary tract nucleus Dorsal vagal nucleus Solitary tract nucleus Dorsal vagal nucleus X XII hypoglossal nuclei

WALLENBERG’S SYNDROME LESIONS OF MEDULLA WALLENBERG’S SYNDROME Lesions that predominately affect the more lateral or dorsolateral portions of the medulla may produce a Wallenberg’s syndrome. Involvement of the spinothalamic tracts (contralateral loss of pain and temperature) with ipsilateral decrease of pain and temperature in the face as a result of damage to the nucleus and tract of cranial nerve V. Nucleus ambiguus involvement gives difficulty in swallowing and phonating (nucleus ambiguus supplies motor impulses to the soft palate, pharynx, and larynx). Damage to the inferior cerebellar peduncle results in ipsilateral ataxia and hypotonia.

HORNER’S SYNDROME Weber's syndrome LESIONS OF MEDULLA HORNER’S SYNDROME Involvement of the sympathetic pathways produces a Horner’s syndrome, which includes a small (constricted) pupil, ptosis, and a dry face (anhidrosis) ipsilateral to the lesion with or without nystagmus if the vestibular nuclei are involved. Weber's syndrome 1 CNXII 2 Nucleus ambiguous 3 Nucleus of spinal tract V 4 Spinal tract of V 5 CN X 6 Restiform body 7Solitary nucleus 8 Dorsal nucleus of X 9 4th ventricle

MEDIAL MEDULLARY SYNDROME LESIONS OF MEDULLA MEDIAL MEDULLARY SYNDROME Déjérine syndrome Déjérine syndrome is due to malperfusion in the territory of the anteromedial group of medullary arteries arising from the vertebral or anterior spinal artery and leads to (a) contralateral hemiplegia (b) dysarthria (inferior olivary nucleus, nucleus ambiguus), (c) decreased proprioception (medial lemniscus), (d) nystagmus (medial longitudinal fascicle), and (e) ipsilateral tongue paresis (hypoglossal nerve).

CONCLUSION The posterior fossa is home for cranial nerve nuclei and many efferent and afferent fiber tracts, therefore any lesion in this region can cause multiple cranial palsy in addition to the sensory and motor deficit. Anatomy of this region is complex and more so the vascular anatomy. In addition wide congenital variation and extensive collateral of vessels make boundaries ill-defined. In the era where we get very limited clinical information and examination findings it becomes more and more important for radiologist to get familiarize with the anatomy and syndromic lesions. And best way to achieve this is repeated revision.

THANK YOU a Penn State presentation skanekar@hmc.psu.edu 11