1. Differential diagnosis for PICA
MRI at acute presentation
MRI after 4 weeks
PRES involving cerebellar hemispheres bilaterally. Bilateral almost symmetrical hyperintensities involving postero-inferior aspect of cerebellum. Findings completely resolved after 4 weeks on follow up MRI

2. (superior cerebellar artery syndrome).
SCA Syndrome
(superior cerebellar artery syndrome).
Main symptoms are ipsilateral cerebellar ataxias (middle and/or superior cerebellar peduncles), nausea and vomiting, slurred (pseudobulbar) speech, loss of pain and temperature over the opposite side of the body. Partial deafness, tremor of the upper extremity, an ipsilateral Horner syndrome and palatal myoclonus have been reported. Clinically, this stroke may be impossible to distinguish from a partial AICA or PICA territory stroke. It is much rarer than either one. Ocular pulsion away from the side of lesion has been reported in SCA syndrome.
SCA territory infarction due to basilar artery thrombosis

3. (superior cerebellar artery syndrome).
SCA Syndrome
(superior cerebellar artery syndrome).
SCA infarct includes the entire superior aspect of the cerebellar hemisphere, the ipsilateral superior vermis, and variable amounts of the deep white matter. Most of the dentate nuclei are also involved.

4. anterior inferior cerebellar artery syndrome
AICA
anterior inferior cerebellar artery syndrome
The AICA syndrome is usually accompanied by vertigo and unilateral ipsilateral deafness from labyrinthine artery ischemia, ipsilateral facial weakness and ataxia. It is the second most common brainstem stroke, after PICA stroke. The distribution of the classical AlCA infarction involves the lateroinferior pons; middle cerebellar peduncle; flocculus; and a small portion of the anterior, medial, and inferior aspects of the cerebellar hemisphere. The extent of this stroke is extremely variable. S/S: fluctuating hearing, tinnitus, vertigo. Bilaterality of hearing fluctuation suggests a vascular cause.

5. Basilar artery thrombosis & infarction patterns

6. LESIONS OF MIDBRAIN
Infarcts of the brain stem reflect the vascular supply. Infarcts are either paramedian or lateral and, less commonly, dorsal. Most infarcts at the level of the pons and medulla are unilateral, paramedian, and sharply marginated at the midline, with the long axis of the lesion directed sagittally. This orientation reflects the distribution of the paramedian penetrating branches of the basilar and distal vertebral arteries, which perforate the paramedian brain stem and never cross the midline. Midbrain infarctions are usually the result of occlusion of the posterior cerebral artery or occlusion of some of the numerous penetrating branches that supply the midbrain. Most of the infarcts in this region are small, midline, or paramedian foci and were difficult to correlate with specific clinical symptoms.

7. LESIONS OF MIDBRAIN
WEBER’S SYNDROME
Ipsilateral oculomotor palsy contralateral hemiplegia.
A unilateral lesion that affects the ventral portion of the mesencephalon will likely involve the cerebral peduncles (including the corticospinal and corticobulbar tracts), and thus may result in a complete or partial contralateral hemiparesis or hemiplegia without accompanying sensory disturbances. Because the oculomotor nerve (III) exits the midbrain anteriorly. third nerve palsy on the same side as the lesion. Signs of third nerve involvement may include dilated pupil, ptosis (weakness and partial closure of the eyelid), and difficulty looking up, down, or toward the midline in the affected eye.
Ipsilateral oculomotor palsy contralateral hemiplegia.

8. LESIONS OF MIDBRAIN
BENEDIKT’S SYNDROME
Ipsilateral oculomotor palsy. Contralateral hemiplegia. Contralateral tremor
If a unilateral lesion is confined to the middle or tegmental region of the midbrain, critical structures such as red nucleus, the medial lemniscus (and dorsally located spinothalamic tracts), III nerve complex, and crossing fibers from the superior cerebellar peduncle will get affected. C/F: III nerve involvement (ipsilateral dilated pupil, ptosis, and restricted eye movement), one may find contralateral face and hemibody sensory symptoms. Involvement of the red nucleus and superior cerebellar peduncle may result in ataxia and tremors on the contralateral side.
Red nucleus
Ipsilateral oculomotor palsy. Contralateral hemiplegia. Contralateral tremor.

9. INTERNUCLEAR OPHTHALMOPLEGIA
LESIONS OF MIDBRAIN
INTERNUCLEAR OPHTHALMOPLEGIA
Periaqueductal and III nucleus infarction presenting with internuclear ophthalmoplegia after cardiac catheterization.
For normal synchronous eye movements, cranial nerves III, IV and VI communicate through the medial longitudinal fasciculus (MLF), the neural pathway connecting the cranial nerve nuclei responsible for eye movements. In INO, a lesion disrupts this pathway, preventing communication between cranial nerves. The etiology of INO/BINO is most commonly multiple sclerosis. There is a painless onset of visual disturbance, but often no diplopia in primary gaze. There will be horizontal diplopia in lateral gaze. The patient will manifest an adduction deficit on the involved side and a nystagmus of the fellow eye in extreme abduction. 9

10. LESIONS OF MIDBRAIN
PARINAUD’S SYNDROME
upward gaze and convergence palsy with pupillary and eye movement abnormalities
Tumors of the pineal gland can compress both the superior colliculi and pretectum and to the Edinger–Westphal nuclei (rostral part of the oculomotor nuclear complex that is responsible for pupillary constriction). Such lesions typically will result in disturbances of conjugate upward gaze and pupillary changes (the pupils will react sluggishly to light but will constrict on accommodation). This disorder is known as Parinaud’s syndrome.
Pilocystic astrocytoma: Paralysis of upward gaze and convergence, often accompanied by other pupillary and eye movement abnormalities.

11. VENTRAL PONS INFARCTION
LESIONS OF MIDBRAIN
VENTRAL PONS INFARCTION
Lesions affecting the ventral portion of the pons likely will affect the descending corticospinal and corticobulbar tracts resulting in a contralateral hemiparesis or hemiplegia, including the muscles of expression of the lower face. A more expansive lesion in the pons may affect the trigeminal nerve, resulting in ipsilateral sensory losses in the face, including an absent or diminished corneal reflex and ipsilateral weakness of the lower jaw.