Neurological exam

Ocular bobbing and ocular dipping
The literature is rife with confusing terminology for these disorders. Details including videos are below, but here is a chart to help.

Ocular bobbing
Fast down, slow back up to midgaze, usually due to intrinsic pontine lesions. C. Miller Fisher first discussed this phenomenon at a conference in 1959, and wrote about it in more detail in 1964, describing three case of patients in whom the eyes would briskly dip downward several millimeters and then return to their primary position in a "bobbing" action. The downward movement is faster than the upward and usually only goes down 1/4th to 1/3rd of the normal full voluntary movement. It is generally associated with pontine hemorrhage or infarction. The movements are usually conjugate and of limited excursion, but can be more downward in one eye than the other, and often beat at an irregular frequency. It localizes fairly well to the intrinsic pons when "typical" (meaning when all lateral eye movements are impaired but vertical eye movements are okay), but has also been reported from cerebellar hemorrhagic infarction in this setting. When some degree of horizontal eye movements is preserved it is more commonly due to alternative etiologies such as cerebellar hemorrhage, obstructive hydrocephalus, or metabolic encephalopathy.

It can occur in other brainstem injury such as extrinsic compression when some degree of horizontal eye movements are preserved. It also can be monocular, which occurs when there is a coexisting oculomotor palsy. Some of hypothesized that, at least in some patients, this may result from being the only residual eye movement in patients with impairment of all other eye movements.

Video: Neuro-Ophthalmology Virtual Education Library, Daroff Collection at http://www.kaltura.com/index.php/extwidget/preview/partner_id/797802/uiconf_id/27472092/entry_id/0_ilda2lhm/embed/auto?

Video: Neuro-Ophthalmology Virtual Education Library, Cogan Collection at https://collections.lib.utah.edu/ark:/87278/s6ff3v1z

Associated disorders
 * Pontine hemorrhage or infarction (most commonly)
 * Obstructive hydrocephalus
 * Cerebellar hemorrhage
 * Subarachnoid hemorrhage anterior to the brainstem
 * Metabolic encephalopathy
 * Leigh syndrome
 * Traumatic brain injury
 * Bromide intoxication
 * Brainstem encephalitis
 * Osmotic demyelination (central pontine myelinolysis)
 * Organophosphate poisoning

Reverse ocular bobbing
Fast up, slow back down to midgaze, usually due to metabolic encephalopathies. Daroff et al. first reported on these movements in Glaser's textbook of Neuro-ophthalmology in 1978, describing the eyes initially quickly jerking upwards and then slowly returning to the horizontal, associated with metabolic encephalopathy. It has been reported in two patients intoxicated concurrently with both benzodiazepines and phenothiazines. It has also been reported in a child with tuberous sclerosis.

Associated disorders
 * Metabolic encephalopathy
 * Specific overdoses: benzodiazepines and phenothiazines
 * Tuberous sclerosis

Ocular dipping
Slow down to the limit of gaze, fast back up to midgaze, usually due to hypoxic-ischemic encephalopathy but can occur in many other causes Knobler et al. first described these movement in 1981 as "inverse ocular bobbing" in two patients with status epilepticus. Allan Ropper first coined the term "ocular dipping" in 1981 and described the disorder in more detail as a pattern of conjugate slow downward eye drift, brief pause, and then rapid return to primary position in patients with anoxic brain injury. Horizontal eye movements were preserved. Unlike ocular bobbing, the downward movement was down to the extreme limit of downward gaze, and the movement down was slow with a fast return back up. There were no seizures on EEG. In some patients who improve from anoxic coma, these movements go away, so they do not signal a definite ominous prognosis. The movements can be aggravated by noxious stimuli or passive limb movements.

Video: (JN Learning, https://edhub.ama-assn.org/jn-learning/video-player/17782355)

Video: Neuro-Ophthalmology Virtual Education Library, Wray Collection: https://collections.lib.utah.edu/ark:/87278/s6k9653k

Associated disorders
 * Hypoxic-ischemic encephalopathy (most commonly)
 * Seizures
 * Post-anoxic myoclonus
 * Pontine infarction
 * Creutzfeldt-Jakob disease
 * Uncal herniation
 * Anti-NMDA receptor antibody encephalitis
 * Pinealoblastoma
 * Acute encephalitis
 * Traumatic brain injury
 * Wernicke's encephalopathy
 * Hemiplegic migraine from CACNA1A mutation

Reverse ocular dipping
Slow up, fast back down to midgaze, patients usually awake, in encephalitis or toxic-metabolic. In 1987, Goldschmidt and Wall first described this movement of slow upward deviation followed by a rapid return to midposition in a 59 year old patient with a brainstem infarct who was otherwise awake, and called it "slow upward ocular bobbing." Then, in 1988 Titer and Laureno desribed similar movements in a patient intoxicated with carbamazepine and lithium who was not comatose and called it "inverse/reverse bobbing." Rehman and Mehler described this later in 1988 and called it "reverse ocular dipping." This patient had cryptococcal meningitis and was awake and partially responsive, with intact oculocephalic and caloric responses. It is unclear if the disorder was due to the meningitis, a metabolic encephalopathy, or an alternative etiology. In 1994 Toda et al. described similar findings in an awake patient with pneumonia and Parkinson disease, who was similarly awake and responsive (this case was described as "slow-upward ocular bobbing" but it is actually reverse ocular dipping. In 2014 a case was described in a patient on fentanyl and droperidol, which resolved after the drugs were held.  The patient was similarly awake during it. In 2016 a case was described of a patient with CSF leak causing intracranial hypotension with this associated syndrome along with a decline in consciousness.

Video: (Neurology Journal, https://www.youtube.com/watch?v=YuJ4iwHjhw8

Video: BMJ Case Reports, https://casereports.bmj.com/content/2014/bcr-2014-206951

Associated disorders:
 * Specific overdoses: carbamazepine and lithium, and fentanyl and droperidol
 * Metabolic encephalopathy
 * Brainstem infarction
 * Intracranial hypotension
 * Meningitis (possibly)