Download (superior cerebellar artery syndrome).

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
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
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.
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.
Basilar artery thrombosis & infarction patterns
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.
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.
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.
INTERNUCLEAR OPHTHALMOPLEGIA
LESIONS OF MIDBRAIN
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.
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.
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.