a presentation to hospital with vertigo or dizziness is common [ 1 , 2 ] . the usual 
 reason is disabling dizziness leading to nausea , vomiting , and often prostration 
 or inability to mobilise . patients with these symptoms are 
 challenging with difficulty determining which specialty to refer to . otolaryngologists have expertise 
 in this area ; however , patients may be more appropriately referred to neurologists 
 or general physicians in the first instance . we discuss the close interplay of pathophysiology relating to vertigo , 
 nystagmus , oscillopsia , and the vestibulo - ocular reflex and its modulation by 
 head titubation . it may be induced by stimulation of the intact sensorimotor system or 
 by dysfunction of any of the stabilising sensory systems . general sensations of dizziness , in contrast , are often of 
 nonvestibular aetiology . whether this be an impending 
 faint ( type ii ) , dysequilibrium ( type iii ) , or vague lightheadedness ( type 
 iv ) , it may be due to nonvestibular causes . these can include cerebrovascular 
 disease , multiple sclerosis , cns tumours , migraine , or epilepsy . a sixty - four - year - old lady presented to her general practitioner 
 ( gp ) with acute onset of unsteadiness and dizziness associated with movement . she 
 visited her doctor with a complaint of feeling dizzy and faint but had a blood 
 pressure of 113/70 mmhg . she had no abnormalities on general , vestibular , 
 neurological , and otological examinations , 
 including no nystagmus . the dizziness was described as repeated attacks of a sensation 
 of internal moving ; that is the patient was  whirling  , but the room was still . her symptoms worsened over the 
 following week , disturbing her daily activity and leading to nausea , vomiting , 
 and prostration . the gp had noted that she had irregular and erratic eye 
 movement and had developed a postural drop in her blood pressure , from 
 113/70 mmhg to 97/63 mmhg on standing . a week later she was permanently dizzy and nauseous and had noticed 
 some difficulty in pronunciation of words . the dizziness was now described as a 
 constant sensation that she was turning and tilting over , when she knew she was 
 upright , and the room was still . there had also 
 been the occasional sensation that the room was spinning around , although these 
 were the only fleeting . she had no visual disturbance , hearing problems , weakness 
 or numbness , and her neurological examination was normal . she was treated with antiemetics including 
 prochlorperazine ; with a presumed diagnosis of vestibular failure , and her gp referred 
 her to the otolaryngology services for further treatment and to investigate for 
 an organic cause . on admission on 
 examination , she was noted to have a subtle head nodding tremor or titubation . this was associated with a low - frequency tremor of the upper limbs , which appeared 
 to increase on intention . she had erratic eye movements and it was very difficult to elicit any 
 nystagmus , even with frenzel glasses , whether spontaneous or positional . this 
 was due to the difficulty in keeping her eyes open secondary to overwhelming 
 nausea . the patient found that 
 it very difficult to keep her eyes still and to focus on a stationary object 
 and she was unable to smoothly pursue a moving target . there was clearly a 
 fixation instability and it appeared to be in the form of conjugate involuntary 
 saccadic oscillations . there was , however , a fleeting vertical nystagmus on upgaze , which may have 
 indicated a gaze - evoked cause , but with no obvious horizontal element . a halmagyi - curthoys head thrust test was 
 attempted , but proved difficult to interpret due to the stimulation of 
 vomiting . it was noted , however , that the patient was unable to fix on a 
 stationary object during head rotation indicating a probable suppression of the 
 vestibulo - ocular reflex ( vor ) . due to 
 the significant nausea and vomiting , a caloric canal test was not performed . she had subtle 
 cerebellar signs on subsequent examination , including dysmetria and 
 dysdiadocokinesis . dix - halpike test was symptomatically 
 positive , with vomiting but with no rotatory nystagmus and no positional 
 dependence . she was given 
 intravenous fluids and steroids and treated symptomatically for the nausea and 
 vomiting . it was 
 postulated that there was a central cause for her symptoms , due to the 
 combination of cerebellar signs , fixation instability / opsoclonus , possible 
 upbeat nystagmus , and vor suppression . therefore , a magnetic resonance scan ( mri ) 
 of the brain was ordered . this revealed a large space - occupying lesion in the 
 right lobe of the cerebellum , with a smaller lesion in the left lobe ( figure 1 ) . the patient was referred directly to the neurosurgeons who performed a 
 suboccipital craniectomy and excision of the cerebellar tumour . as a presentation to otolaryngology , the history of this case is not 
 unusual . , it accounts for 13% of patients , but only 50% of those referred to 
 otolaryngology services have an otological cause for their symptoms . it can be argued , therefore , that patients presenting with these symptoms should 
 be referred to general physicians in the first instance , to rule out serious 
 nonotological causes . the anamnesis of dizzy symptoms is especially important to elicit in 
 detail in order to make informed decisions on referral route . vertigo indicates a sensation of false movement ( generally 
 described like a rotation ) , but rarely , the patient can describe it like a sensation 
 of tilt . in our case , the patient described both rotational and tilting sensations , whilst stationary and on 
 movement . most importantly was the constant sensation that she was turning but 
 that the room was still . this specific symptom , and its duration , 
 indicates an increased risk of central origin . with peripheral vestibular causes of vertigo this may be a result 
 of oscillopsia , an optical illusion of oscillation sometimes as a direct result 
 of nystagmus . oscillopsia is common in bilateral 
 labyrinthine abnormality , but the presence of vertical oscillopsia indicates a 
 vertical nystagmus , which is indicative of a central lesion . in this case , spontaneous 
 nystagmus , albeit fleeting , was vertical nystagmus and this is particularly 
 specific to central lesions rather than peripheral vestibular lesions , and is a 
 reliable indicator . damage to the ventral 
 tegmental tract , originating in the superior vestibular nucleus , leads to 
 upward vestibular signals to the third nerve nucleus and so upbeat nystagmus 
 ( ubn ) . therefore , 
 a vertical nystagmus should give high index of suspicion for a central cause . the general inability to stabilise the eye , 
 resulting in the erratic eye movement and opsoclonus seen may also indicate 
 central pathology . particular regions involved are the vermis , flocculus , and paraflocculus , which 
 are responsible for coordinating smooth pursuit and adaptation of the 
 vestibulo - ocular reflex ( vor ) . these control mechanisms are essential to holding the eye steady for 
 fixation , both immediately after saccades and in eccentric positions of gaze , particularly 
 important when attempting to track a moving target . the lesions in the cerebellum 
 may well have impaired these important mechanisms in this patient , leading to opsoclonus 
 and an inability to fixate . it is also known that an impairment of adaptation 
 of the vor , to compensate for movement , may lead to oscillopsia . although 
 the lesions seen on mri in this case are not in the vermis , surrounding oedema 
 and paraneoplastic effects may be responsible for an impairment of vermis 
 function . the general difficulty in diagnosis , detailed 
 neurotologic examination , and testing in this case may have been influenced by 
 the use of prochlorperazine . this is a phenothiazine antipsychotic agent which 
 is very commonly used as a vestibular sedative for nausea due to vertigo . it is 
 widely known , however , although affording symptomatic relief for the patient , 
 this drug can result in a delay to vestibular compensation and influence 
 diagnostic testing . this is 
 defined as nodding head tremor with a frequency of 3 to 4 hz and may be seen in 
 midline cerebellar disease [ 12 , 13 ] . titubation can occur in isolation or 
 combined with a postural tremor elsewhere , especially in the arms . this can be 
 seen in patients with essential tremor or dystonic tremor , associated with 
 posterior fossa disorders . essential tremor , such as this , is closely related 
 to the oculomotor deficits described above . these include deficits of pursuit 
 initiation and suppression of the vor . it has been shown that there is a strong 
 correlation with the intensity of intention tremor and the oculomotor 
 impairment and may indicate an impairment of the caudal cerebellar vermis . there is the potential , however , that the tremor and head titubation may have 
 been an extrapyramidal akathisia as a result of prochlorperazine use . the closely related interplay of the mechanisms involved in this 
 patient 's symptoms are 
 difficult to sequence . the cerebellar lesions are the only true evidence of a 
 causal element to this case . however , it remains to be understood how these 
 lesions had brought about the specific symptom complex identified . was the 
 vertigo a direct result of the lesion or was it secondary to an oscillopsia 
 generated by nystagmus , or due to failure of the vor ? was ubn or gaze - evoked nystagmus present , or was it just 
 a brief recognisable pattern in the otherwise erratic oculomotor impairment or 
 opsoclonus , or secondary to loss of adaptation of the vor ? was the head 
 titubation the key ? oscillopsia occurs when there is failure of the vor to 
 adapt and compensate for head movements . cerebellar lesions may impair the 
 normal cerebellar adaptive mechanism for the vor and so impair its ability to 
 compensate for movement of the head . simultaneously , a cerebellar lesion may 
 also lead to an essential tremor , manifesting as head titubation and upper limb 
 tremor . many of the signs seen in this case , such as the impaired vor , the 
 titubation , opsoclonus , and dysarthria , are classically caused by cerebellar 
 vermal lesions . however , the lesions seen on mri are in the deeper hemispheres . 
 one may , therefore , suggest that surrounding oedema and local compression have led to 
 vermal damage . it can be seen in figure 1 that there is a degree of cerebellar midline shift . one may conclude that the lesions themselves may have 
 simultaneously caused a tremor and an inability for the vor to compensate for 
 it . oscillopsia due to an impaired vor has been shown to be more likely than oscillopsia due to a titubation .   also , the two cerebellar lesions may have had 
 the two separate effects of tremor and impaired vor . 
			  the differentiation between central and peripheral causes of vertigo 
 can be perplexing and often require the expertise of a specialist 
 neurotologist . many signs and tests , such as saccadic pursuit , gaze - evoked 
 nystagmus , and the halmagyi - curthoys test , have recently been shown to be 
 unreliable in distinguishing peripheral from central causes ; therefore , an 
 expert opinion may be required . however , whether the vertigo in this case was 
 a result of an oscillopsia , nystagmus , or central cause , the referral route 
 should initially be via a general physician to rule out such life threatening 
 causes as central tumours . suspicion of a 
 central cause for vertigo on examination should prompt urgent imaging of the 
 central nervous system.a vertical nystagmus should give high index of suspicion for a central 
 cause.central vestibular lesions may present with a wide variety of symptoms and signs which 
 may include impaired vor , head titubation and tremor , opsoclonus , and oscillopsia.initial referral 
 of patients with disabling vertigo should be via general physicians . suspicion of a 
 central cause for vertigo on examination should prompt urgent imaging of the 
 central nervous system . central vestibular lesions may present with a wide variety of symptoms and signs which 
 may include impaired vor , head titubation and tremor , opsoclonus , and oscillopsia .
objective . discuss complex interplay of pathophysiological effects of cerebellar space occupying lesions on the vestibular pathway . 
 discuss challenges of diagnosis and referral along with differential and final diagnosis of unusual presentation . 
 case report . 
 we describe the case of a patient with vertiginous symptoms complicated by neurological features , namely , head titubation and tremor . 
 the patient also had signs of oscillopsia and possible impairment of the vestibulo - ocular reflex . the resulting symptom and sign complex made for a difficult diagnosis , as the interplay of the pathophysiology of these signs , were unusual . conclusion . 
 the discussion has revealed that the cerebellar lesions themselves may have simultaneously caused head tremor and an inability for the vestibulo - ocular reflex to compensate , resulting in vertigo . 
 however , whether the vertigo was a result of an oscillopsia , nystagmus , or central cause , the referral route should initially be via a general physician to rule out such a life threatening cause as a tumour .