Journal of Neurology, Neurosurgery, and Psychiatry 1985;48:263-265 Small cerebellar strokes may mimic labyrinthine lesions CY HUANG, YL YU From the Department ofMedicine, University ofHong Kong, Queen Mary Hospital, Hong Kong SUMMARY Thirty nine cases of cerebellar infarct and haemorrhage were seen over a period of 3 years. Of these, 69% had no impairment of consciousness. Six cases had nystagmus and gait ataxia as their only abnormal signs. Small cerebellar strokes may present with only vertigo, unsteady gait, and unidirectional nystagmus, thus mimicking labrynthine lesions. Care in managing vertigo attacks in patients with risk factors for cerebrovascular disease appears to be warranted. Until the advent of computed tomography, cerebellar infarction and haemorrhage were thought to be rare, and were seldom diagnosed in life.' 2 Although now better recognised, recent reviews3 nevertheless continue to emphasise the more severe cases. We review our experience in the last 3 years, both to document that cerebellar haemorrhage and infarcts are not rare and also to emphasise that small cerebellar infarction and haemorrhage may mimic more benign lesions. Cases Nineteen patients (11 males, eight females age 43-80 years) with cerebellar infarction, and 20 patients (eight males, 12 females age 45-73 years) with cerebellar haemorrhage were seen in the University Medical Unit, Queen Mary Hospital from January 1981 to December 1983. All diagnoses were confirmed on CT scan, 48-6% of which was performed within the first 3 days, and 86-6% within the first 9 days. Fifteen of the infarct cases, and 12 of the haemorrhage cases had no disturbance of consciousness during the course of their illness. This group of 27 patients had fairly similar features of vertigo, nystagmus, nausea and vomiting, unsteady gait and limb ataxia. Headache was infrequent, as also were limb weakness and cranial nerve abnormality (table 1). The vertigo was spontaneous and lasted for more than 5 minutes at onset in all cases, Address for reprint requests: Dr CY Huang, Department of Medicine, University of Hong Kong, Queen Mary Hospital, Hong Kong. Received 1 May 1984 and in revised form 31 July 1984. Accepted 6 August 1984 although brief vertigo of seconds duration precipitated by head movements, occurred later in three patients. Nystagmus was unidirectional in six cases of infarct, and three cases of haemorrhage. This was in the same direction as the direction of fall in two cases, and opposite in three cases. In the other four cases the patients had no consistent direction of falling. The direction of nystagmus did not lateralise the lesion well, corresponding in four of the unidirectional cases and not corresponding in five cases. Six cases had nystagmus and gait ataxia as their only abnormal signs (table 2). However, careful examination revealed history of dysarthria in one, and presence of upgaze nystagmus in another. Most of the patients in this group resumed normal walking within a few days. Twelve other cases had disturbance of consciousness. Of these 12 cases, three cerebellar haemorTable 1 Symptoms and signs ofbenign cerebellar stroke Haemorrhage Infarct Patient number Symptoms Abnormal mental state Headache Vertigo Unsteadiness Dysarthria nausea/vomiting 15 12 0 1 8 12 3 9 0 3 9 11 2 10 Gait ataxia Limb ataxia Nystagmus Limb weakness Hearing disturbance/tinnitus Ocular movement abnormality Other cranial nerve abnormality Sensory loss 15 8 8 1 2 3 12 9 5 2 0 3 0 1 3 0 Signs 263 Huang, Yu 264 Table 2 Minimal feature cerebellar stroke Clinical feature Sex Age (yr) 1 M/60 2 M/56 3 4 M/59 M/65 5 F/55 6 F/72 Vertigo, nausea, gait ataxia, left beating nystagmus, transient left hearing defect Vertigo, nausea, gait ataxia, nystagmus to right Vertigo, nausea, gait ataxia Transient dysarthria and vomiting, gait ataxia Nausea, vomiting, vertigo, nystagmus on left gaze and upgaze, gait ataxia Vertigo, right beating nystagmus, gait ataxia CT finding Right cerebellar infarct Left cerebellar infact Right cerebellar infarct Right cerebellar infarct Left cerebellar infarct Right cerebellar haemorrhage rhage cases required operation, one refused surgery and died suddenly on the 17th day. Of the infarction cases, one died before surgery could be performed and one died with brainstem infarction. The others did not need surgery. Among the entire group of cerebellar stroke, hypertension was present in 10 of the infarcts, diabetes mellitus in four. Fourteen of the haemorrhages had hypertension, and two had diabetes. Previous stroke or TIA was not recorded in any ischaemic cases, but one of the haemorrhage cases had had a previous lacunar infarct and another had had an episode of spontaneous vertigo 2 years previously. Fig 1 Small infarct in the right cerebellar nemispnere. Illustrative cases Case I A 60-year-old male Chinese was known to be hypertensive but not treated for 2 years. He suddenly developed on the day of admission, severe vertigo, unsteadiness, nausea and vomiting. The vertigo lasted for one hour and was accompanied by transient left hearing difficulties but not tinnitus. Afterwards, head movement would precipitate brief vertigo. There was no headache or other symptoms. On admission, he was mentally alert, with a blood pressure of 160/100 mm Hg. He had nystagmus with fast component to the right on right gaze. There was no dysarthria or limb ataxia. However, he was unable to walk except with a wide-based gait. The rest of his neurological examination was normal. CT scan demonstrated an area of decreased attenuation in the right cerebellar hemisphere (fig 1). His condition improved and he was able to walk normally in a few days. Case 5 A 55-year-old Chinese female had been treated for diabetes mellitus for 7 years. She suddenly developed spontaneous vertigo, and vomiting on the day of admission. Subsequently, vertigo occurred when she turned to the left. On admission she had vertical nystagmus on upgaze which disappeared after a day, as well as nystagmus with fast component to the left on left gaze. There was no limb ataxia. She tended to fall to the right when she tried to Fig 2 Small infarct in the left cerebellar hemisphere. walk. No other abnormality was detected. CT scan showed a left cerebellar hemisphere infarct (fig 2). The gait became normal after a few weeks. Small cerebellar strokes may mimic labyrinthine lesions 265 cerebellar transient ischaemic attacks, as well as Discussion small infarcts may have no features other than verDescriptions of symptoms and signs in cerebellar tigo, unidirectional horizontal nystagmus and infarction and haemorrhage in earlier necropsy unsteadiness, and therefore be misdiagnosed as series emphasised gross and dramatic deficits. Sypert benign labyrinthine lesions. Since vertigo alone is and Alvoid' noted that 64% of their patients with more likely to be due to labyrinthine disease, current cerebellar infarction had abnormal mental state, practice rightly does not consider transient vertigo 47% ocular movement abnormality, 42% motor dis- and unsteadiness per se as diagnostic of vertebroturbance, and 57% had other cranial nerve abnor- basilar TIA. Nevertheless, cases of vertigo occurring mality. Ott et a!2 described headache, nausea, vomit- in patients with risk factors for cerebrovascular dising, unsteadiness in most of the patients with cere- ease should perhaps be investigated for this possibellar haemorrhage, and only 14 of their 56 patients bility more often than currently practised, especially when the vertigo is not positional related at onset, were alert. Seventy three per cent of the patients had limb ataxia, ipsilateral gaze palsy and and unaccompanied by tinnitus and hearing disturperipheral facial palsy. However, later studies using bance. Ott et al commented that 52% of cerebellar computed tomography detected less dramatic presentations. Scotti et a14 described 21 cases of cerebel- haemorrhage patients who were awake for 2 days lar infarction of which 15 had a benign course. Men- later deteriorated.2 In our cases about a fifth of the tal abnormality was detected at admission in only infarction cases did show progressive stepwise six of the cases. Ocular movement disorder was seen deterioration. Whether early initiation of antiin six of 21 cases, facial palsy in eight, and limb coagulant therapy could prevent this deterioration is weakness in eight. Ho et al! described another seven uncertain. However, Scotti et a!4 had earlier concluded that no symptoms or signs differentiated cases of which one needed surgery. The current series documents that cerebellar infarction and cerebellar infarct or haemorrhage with certainty, haemorrhages are not rare and many present with except perhaps headache. Our experience would unsteadiness, vertigo, nausea, and vomiting, with lit- concur with this. Even among the six patients who tle disturbance of consciousness, cranial nerve palsy, presented with the minimal features of vertigo, nausea, nystagmus and ataxic gait, there was one or limb weakness. Signs of brainstem abnormality such as vertical nystagmus and diplopia may be case of cerebellar haemorrhage. Significant transient and subtle. The gait ataxia can easily be headache was so uncommon with small cerebellar blamed on labyrinthine disturbance alone. The fea- haemorrhages that this symptom also becomes tures therefore easily mimic those of labyrinthine unhelpful. Computed tomography should therefore disturbance. This possibility of misdiagnosing cere- be used before any anticoagulation is initiated. bellar lesions for more benign peripheral disorders has previously been noted by Duncan et al,6 who References described three cases of acute cerebellar infarction in the PICA territory where the patients had only 'Sypert GW, Alvord EC. Cerebellar infarction. A clinicopathological Arch study. positional related dizziness, nausea, vomiting and Neurol 1975;32:357-63. unsteadiness. The nystagmus was unidirectional in 2 Ott KH, Kase CS, Ojemann RG, Mohr JP. Cerebellar two cases. They thought that a nystagmus in the hemorrhage: diagnosis and treatment. A review of 56 opposite direction to the falling would favour cases. Arch Neurol 1974;31:160-7. labyrinthine lesion. In our cases, however, reliance 3Heros RC. Cerebellar hemorrhage and infarction. Stroke on the relationship of the direction of fall to that of 1982; 13(1): 106-9. the nystagmus would have led to erroneous diag- 4Scotti G, Spinnler H, Sterzi R, Vallar G. Cerebellar nosis in three out of five cases. softening. Ann Neurol 1980;8: 133-40. Postmortem studies have shown that cerebellar Ho SU, Kim KS, Berenberg RA, Ho HT. Cerebellar infarction: a clinical and CT study. Surg Neurol infarction may not be accompanied by brainstem 1981; 16:350-2. strokes in about 70% of cases.' We have noted earlier that cases of spontaneous non-positional related 6 Duncan GW, Parker SW, Fisher CM. Acute cerebellar infarction in the PICA territory. Arch Neurol vertigo, who develop subsequent cerebrovascular 1975;32:364-8. disease, were more likely to have vertebrobasilar ' Huang CY. Isolated vertigo attacks in patients with territory strokes than carotid territory strokes.' cerebrovascular disease. Excerpta Medica ICS Others have noted that there is increased risk of 1981; 10:548. cerebrovascular disease associated with the less 8 Wilkinson WE, Heyman A, Burch JG. Use of self specific complaint of dizziness.8 The current series administered questionnaire for detection of transient suggests that one possible explanation is that pure cerebral ischaemic attacks. Ann Neurol 1979;6:40-6.