Head-positioning maneuvers can lead to paroxysmal nystagmus and vertigo, which are usually due to a peripheral vestibular disorder like, for example, benign paroxysmal positioning vertigo (BPPV). They are less commonly caused by a central lesion (central paroxysmal positioning nystagmus, cPPV). While many typical features do not permit differentiation between BPPV and cPPV, for example, latency, course, and duration of nystagmus and vertigo during an attack, the direction of nystagmus often does. The nystagmus in BPPV always beats in the direction aligned to the affected semicircular canal plane, i.e., horizontal for the horizontal canal and vertical-torsional for the vertical canals. Any other direction (paroxysmal torsional, upbeat, or downbeat nystagmus) indicates a central origin. Three cases of cPPV exhibiting nystagmus in the latter directions are presented. In one of the cases with paroxysmal downbeat nystagmus and vertigo, all other parts of the neurological examination and brain imaging initially showed no lesion in the posterior fossa. The direction of nystagmus was the only sign that indicated a central origin.

Head positioning can lead to pathological nystagmus and vertigo. In most instances the cause is a peripheral vestibular disorder, as in benign paroxysmal positioning vertigo (BPPV). Central lesions can lead to positional nystagmus (central PN) or to paroxysmal positioning nystagmus and vertigo (central PPV). Lesions in central PPV are often found dorsolateral to the fourth ventricle or in the dorsal vermis. This localization, together with other clinical features (associated cerebellar and oculomotor signs), generally allows one to easily distinguish central PPV from BPPV. However, in individual cases this may prove difficult, since the two syndromes share many features. Even if only BPPV as a peripheral lesion is considered, differentiation based on such features as latency, course, and duration of nystagmus during an attack, fatigability, vertigo, vomiting, and time period during which nystagmus bouts occur, may be impossible. Only the direction of nystagmus during an attack can allow differentiation.

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Background: It is unclear whether sensory symptoms in Parkinson disease (PD) are of primary or of secondary origin attributable to motor symptoms such as rigidity and bradykinesia.Objective: The aim of this study was to elucidate whether sensory abnormalities are present and may precede motor symptoms in familial parkinsonism by characterizing sensory function in symptomatic and asymptomatic PINK1 mutation carriers. Methods: Fourteen family members with PINK1 mutation and 14 healthy controls were examined clinically, with nerve conduction studies and quantitative sensory testing (QST). Results: Thresholds for mechanical detection, mechanical pain and pressure pain were higher in PINK1 mutation carriers compared to controls. Higher thresholds for mechanical detection, mechanical pain and pressure pain were even found in asymptomatic, clinically not or only mildly affected PINK1 mutation carriers. Conclusions: Data suggest that PINK1-associated PD is associated with a primary hypofunction of nociceptive and non-nociceptive afferent systems that can already be found at the time when motor signs of PD are only subtle. As nerve conduction studies did not reveal differences between PINK1 mutation carriers and controls, we propose that the somatosensory impairment is related to abnormal central somatosensory processing.

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