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Published in Terence R. Anthoney, Neuroanatomy and the Neurologic Exam, 2017
In the case of the eyeballs, calling rhythmic involuntary movements “nystagmus” suggests a different set of diagnoses than calling them an ocular “tremor.” It is, of course, possible that all mechanisms capable of producing tremors elsewhere in the body are not capable of producing rhythmic involuntary movements of the eyeballs, and vice versa. If so, then excluding nystagmus from the class “tremor” will not make much practical difference, even if it be semantically and philosophically problematic. But can one ever be sure? That’s the bottom line, and the answer is “no.” In the case of rhythmic involuntary movements of the eyeballs, in fact, there are several statements in recent clinical texts suggestively linking them to rhythmic involuntary movements in other parts of the body.
Arthropod-borne virus encephalitis
Published in Avindra Nath, Joseph R. Berger, Clinical Neurovirology, 2020
There has been a very wide range in the estimated apparent to inapparent infection ratio. A figure of 1:270 has been reported from an endemic region in India after a three-year prospective study [139]. The onset of overt illness follows an incubation period of four to fourteen days. The onset of the first phase of the illness includes fever and chills, headache, and GI symptoms, particularly in children. An undetermined percentage of cases have an uneventful recovery at this stage [136]. Involvement of the CNS evolves with clouding of consciousness, seizures, particularly in children, motor loss and abnormal movements. Meningeal signs can be observed, particularly in adults. In a study of U.S. military personnel in Korea in 1950, Dickerson and colleagues characterized the following findings as pathognomonic: Altered sensorium, mask-like facies, thick retarded speech, coarse ocular tremor, symmetric paresis, and hyperactive deep tendon reflexes [140]. The acute encephalitic phase lasts from one to two weeks, with death, should it occur, frequently found in the third to eighth days [141]. Unusual presentations include a stroke-like illness [142] and acute transverse myelitis [143]. Estimates of fatal outcome range from 10% to 40%, with children under ten years of age the most susceptible. Other indicators of poor prognosis include depth and duration of impaired consciousness, reflex changes, and severity of CSF and EEG abnormalities [135,144]. Only one third of patients fully recover from the encephalitis [135]. The gamut of sequelae includes motor paresis, movement disorders, behavioral abnormalities, mental retardation, and learning disability.
Neuro-ophthalmology of movement disorders
Published in Expert Review of Ophthalmology, 2018
Ocular motility impairment in PD ranges from abnormal (slow, hypometric) saccades and square-wave jerks to convergence insufficiency and upgaze restriction. The latter two ocular signs, although commonly present in patients with PD, are not specific for PD and can be seen in elderly individuals without parkinsonian features. In early stages of PD, reflexive visually guided saccades are usually preserved, but voluntary anti-saccades (saccades in the opposite direction to a stimulus) and memory-guided saccades (saccades for a remembered stimulus that has subsequently disappeared) are impaired [7,8]. In more advanced stages of PD, most patients exhibit different degree of impaired reflexive saccades, smooth ocular pursuit including deficit of smooth pursuit gain, catch-up saccade intrusion, and progressive reduction in displacement of repetitive eye movements similar to decrement in amplitude observed with repetitive motor tasks in PD [9]. Prolonged duration of gaze fixation can be present in PD patients without cognitive impairment, but PD patients with dementia have even longer fixation duration along with further reduction of saccade amplitudes as compared to cognitively intact PD patients [10]. As a result, patients with PD exhibit deficient visual exploration strategies normally consisting of alternating runs of saccades and gaze fixations controlled by cortical and subcortical networks that become involved as part of PD-related neurodegeneration [10]. Convergence insufficiency, characterized by inability to maintain binocular eye alignment on approaching object, is a common ophthalmologic feature of PD and can result in binocular blurring of vision or diplopia, and may impair patient’s ability to read [11,12]. Normal near point of convergence can be seen in early PD but this worsens with disease progression [1,11]. Decreased convergence (measured by placing increasing base-out prism over one eye until a patient can no longer fuse a near target, resulting in diplopia) with or without decreased near point of convergence may be documented in some PD patients [1]. Upgaze restriction is commonly seen in more advanced stages of PD but it usually does not reach the severity of vertical gaze palsy seen in PSP. Ocular tremor (persistent oscillatory eye movements on attempt to fixate on a still object) often has the same frequency as resting limb tremor in PD patients, thus raising the possibility that this sign represents PD tremor involving eyes [13]. Vestibulo-ocular reflex induced by head oscillations due to arm tremor transmitted to the head has been also suggested as a possible mechanism of ocular tremor [14,15].