Cerebellar infarctions
Chapter 8 Cerebellar stroke
Table 8.1 Symptoms in territorial cerebellar infarctions
Symptoms SCA AICA PICA
Deafness Absent Frequent Absent
Dizziness Frequent Absent Frequent
Drowsiness Frequent Frequent Uncommon
Tinnitus Uncommon Frequent Absent
Vertigo Frequent Frequent Very
common Nausea/vomiting Frequent Very
common Frequent
Hallucinations Uncommon Uncommon Absent Headache/facial
pain Uncommon Absent Uncommon
Pain in
limbs/trunk Absent frequent Absent
Sleep
disturbances Uncommon Absent Absent
Abbreviations:AICA: anterior inferior cerebellar artery; PICA: pos- terior inferior cerebellar artery; SCA: superior cerebellar artery.
Figure 8.5illustrates an example of a stroke in the territory of the lateral branch of the superior cerebellar artery.
Border zone infarctions (watershed)
Border zone infarctions are more frequent than pre- sumed (Amarenco et al.,1993). MRI is the technique of choice to identify the lesions, which have an area usu- ally less than 2 cm in diameter (Rodda,1971). Brain
Figure 8.3 Cerebellar venous anatomy.
The Galenic group, the petrosal group, and the posterior group empty into the vein of Galen, the superior/inferior petrosal sinuses, and the straight sinus, respectively. Abbreviations: ANT: anterior;
SUP: superior; POST: posterior; INF: inferior.
With permission from: Blecic and Bogousslavsky,2002.
imaging shows small infarctions mainly found at the boundaries between the SCA and PICA territories, either on the surface of the cortex or around cerebellar nuclei (Amarenco,1995).They are classified in three categories:
! Cortical border zone infarcts are perpendicular to the cerebellar cortex.They are located at the boundary zones between the SCA and PICA territories, or between the PICA and AICA territories.
! Cortical dorsal infarcts are parallel to the cortex, distributed between the SCA and PICA territories.
! Small deep infarcts are located either in the border zone of the AICA and lateral branches of PICA territories, or between the vermal branches of the two SCA arteries.
Clinically, symptoms are similar to those described in SCA, PICA, or AICA infarctions. Symptoms tend to be transient and may be recurrent. Position-related symptoms are common (vertigo, disequilibrium, etc.).
They are probably due to states of low bloodflow in the posterior circulation.
Lacunar infarctions
Lacunar infarctions probably do not exist in the cere- bellum, due to the fact that cerebellar arteries show a progressive reduction in diameter in their course, without penetrating branches arising from middle-size arteries (Fisher,1977).
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Table 8.2 Patterns of posterior inferior cerebellar artery infarctions
Type Incidence Presentation
Dorsal lateral medullary syndrome
(Wallenberg syndrome) 25–30% Vertigo
Nystagmus Ipsilateral Horner sign Appendicular ataxia Cranial nerve palsies (V, IX, X) Contralateral loss of pain/temperature Lateropulsion
PICA infarct sparing brainstem 15–20% Vertigo
Limb and gait ataxia Nystagmus Lateropulsion Headache
Risk of brainstem compression
Isolated acute vertigo 5% Mimics a peripheral labyrinthitis
mPICA 10% Vertigo
Lateropulsion Dysmetria Possible associated Wallenberg syndrome
lPICA 10% Vertigo
Dysmetria
Multiple infarcts 25–30% Multiple infarcts in PICA, AICA, SCA
Possible pseudotumoral presentation Impaired consciousness, coma Abbreviations:AICA: anterior inferior cerebellar artery; PICA: posterior inferior cerebellar artery; SCA: superior cerebellar artery.
Figure 8.4 Anatomical basis of the symptoms in lateral medullary infarction. The lateral region of the medulla (gray zone) is supplied by small perforating branches. Abbreviations: Ambiguous Nc: ambiguous nucleus; Spinothal. Tr: spinothalamic tract; CSP tract: corticospinal tract;
VA: vertebral artery; PICA: posterior inferior cerebellar artery; Trigeminal Nc: trigeminal nucleus; Symp. Fibers: sympathetic fibers; IX–X: cranial nerves IX–X. (Seecolor section.)
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Chapter 8 – Cerebellar stroke
Table 8.3 Patterns of anterior inferior cerebellar artery infarctions
Type Incidence Presentation
Classic syndrome 30–50% Vertigo
Vomiting Tinnitus Dysarthria
Ipsilateral facial palsy Facial sensory loss Horner syndrome Dysmetria Contralateral loss of
sensation Hearing loss Gaze palsy Dysphagia Ipsilateral motor
weakness Isolated vertigo 10–15% Mimics a labyrinthitis
Massive infarction 10% Coma
Tetraplegia Ophthalmoplegia Isolated cerebellar
signs 5%
Figure 8.5 Hyperintense lesion (arrow) in the territory of the lateral branch of the superior cerebellar artery. This patient had a history of abrupt-onset unilateral cerebellar dysmetria with kinetic tremor.
Extra-cerebellar lesions causing hemiataxia
Homolateral ataxia may be accompanied by signs of corticospinal tract involvement in the so-called ataxic hemiparesis (Hiraga et al., 2007).This lacunar syn- drome is associated with lesions in the pons, internal
Table 8.4 Patterns of superior cerebellar artery (SCA) infarctions
Type Incidence Presentation Classical infarct 3–5% Ipsilateral limb dysmetria
Ipsilateral Horner syndrome Contralateral loss of
pain/temperature Sleep disorders
Ipsilateral slow involuntary movements
Hearing loss (uncommon) Contralateral nerve palsy
(IV; rare)
Palatal myoclonus/jaw myoclonus Rostral basilar
artery syndrome
20–25% Diplopia Dizziness Paresthesias Drowsiness Balint syndrome Thalamic-mesencephalic
signs Hemiballism Benedikt syndrome Claude syndrome Weber syndrome Concomitant
infarction in the anterior circulation
Signs of SCA occlusion Aphasia
Brachiofacial weakness
Vestibular form
of SCA Headache
Unsteadiness Dizziness Vomiting Dysarthria Dysmetria Kinetic tremor Nystagmus Lateral SCA
syndrome Ipsilateral limb dysmetria
Axial lateropulsion Dysarthria Nystagmus
Contrapulsion of ocular saccades
Medial SCA
syndrome Gait ataxia
Ataxia of limbs
Increased tone in extensor muscles
Isolated dysarthria Multiple
infarctions Drowsiness, coma
Tetraparesis/tetraplegia Ophthalmoplegia
capsule, corona radiate, and precentral gyrus. Lacunae involve thefibers of the frontopontocerebellar system.
A resulting cerebellar diaschisis can be observed.
Pontine lesions involve the anteromedial pontine arteries. Pontocerebellar fibers disperse among numerous divergent fascicles before converging to
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enter into the contralateral middle cerebellar peduncle (Schmahmann et al.,2004). Contralateral hemiataxia and motor paresis may arise from lesions affecting corticopontine and corticospinal fibers descending close to each other to the midpontine level (Marx et al.,2008).
Lesions at the rostral pontomesencephalic level affect the decussation of the dentate-rubrothalamic pathways as they leave the cerebellum via the upper cerebellar peduncle and cause a bilateral ataxia due to outflow tract impairment (Marx et al.,2008).
Posterior and lateral thalamic stroke can mimic a cerebellar lesion (thalamic ataxia). Patients often show sensory deficits and various degrees of pain according to the location of the stroke. Patients with a thalamic infarct in the territory of the posterior choroidal artery involving the posterior thalamic nuclei may develop delayed complex hyperkinetic motor syndromes, com- bining ataxia, tremor, dystonia, myoclonus, and chorea (“jerky dystonic unsteady hand”) (Ghika et al.,1994).
These patients have sensory dysfunction. Brain MRI shows infarcts in the territory of the posterior cerebral artery involving the posterior choroidal territory, with an abnormal signal in the posterior area of the thala- mus.The other thalamic, subthalamic, and midbrain structures are spared. Dystonia, athetosis, and chorea are associated with position sensory loss, whereas the tremor and myoclonic movements are related to the presence of ataxia (Kim,2001).
Pure or predominant brainstem sensory stroke is most often caused by small infarcts or hemorrhages in the paramedian dorsal pontine area and may be distin- guished from thalamic pure sensory stroke by the fol- lowing features: frequent association of dizziness and gait ataxia, predominant lemniscal sensory symptoms, occasional leg dominance or cheiro-oral pattern, and frequent bilateral perioral involvement (Kim & Bae, 1997).
Outcome of cerebellar infarctions
The pseudotumoral complication with brainstem compression and herniation is a major life-threatening consequence of cerebellar infarctions. Patients develop hydrocephalus, impaired consciousness, and coma.
The compression may develop from a few hours after the stroke up to 8 days after the stroke, although the first 4 days involve greater risk. Full PICA infarc- tions lead to brainstem compression and tonsillar her- niation in 25% of cases (Kase et al.,1993). Isolated
Table 8.5 Mechanisms of cerebellar infarctions Atherosclerosis
Dissection Embolism Hypoperfusion Small artery disease Aneurysm Infection Migraine
AICA infarctions have a more benign course. How- ever, the prognosis of proximal occlusion of the AICA may be worse, since AICA infarcts may herald a mas- sive occlusion of the basilar artery. Full SCA infarc- tions have a pseudotumoral presentation in 20% of cases. Nevertheless, partial SCA infarcts usually have a benign course.This is typically the case in lateral SCA infarction (Barth et al.,1993).