In gaze Palsy (Vertical, Horizontal) disorders, lesions at different levels of the brain spare some of the eye movement systems while affecting others. The resulting pattern of eye movements helps clinicians to localize lesions accurately in the central nervous system.
Common lesions causing gaze palsies include cerebral infarcts, demyelinating lesions, multiple sclerosis, tumors, Wernicke’s encephalopathy, metabolic disorders, and neurodegenerative disorders such as progressive supranuclear palsy.
Evaluation of the different gaze disorders is a bane of most budding neurologists and neurosurgeons. However, a simple and systematic clinical approach to this problem can make their early diagnosis rather easy.
A vertical gaze palsy (VGP) is a conjugate, bilateral, limitation of the eye movements in upgazed and/or downgaze.
Vertical gaze palsy (VGP) can affect functional eye movements by selectively involving the saccadic pathway and may spare or involve spare smooth pursuit or optokinetic movements or non-selectively involve vertical gaze palsy (VGP) for all types of eye movements. Eye movements can also be anatomically classified into supranuclear, nuclear, and infranuclear.
Here I’ll be focus on supranuclear pathways involving three major anatomical structures. Combined bilateral lesions of the nuclear or infranuclear pathways including the neuromuscular junction (e.g., myasthenia gravis, MG) or muscles (e.g., restrictive thyroid ophthalmopathy) can also mimic vertical gaze palsy (VGP) but are usually asymmetric and in contrast to supranuclear VGP cannot be overcome with vestibulo-ocular reflex (VOR) or the doll’s head maneuver.
Multiple sclerosis (MS), known as a chronic inflammatory disease primarily involving the central nervous system, can be presented with various clinical manifestations such as sensory problems, visual disturbances, weakness, gaze abnormalities, etc. with some being more common and others less.
Conjugate gaze deviation is relatively common in ischemic and hemorrhagic stroke and is found in approximately 15%–30% of cases. Anatomically, the frontal eye fields (FEF) located between the premotor and prefrontal cortex are crucial for supranuclear control of horizontal conjugate gaze. Descending FEF fibers project to the paramedian pontine reticular formation (PPRF) in the brainstem, and lesions of this circuit at the paramedian pontine reticular formation (PPRF), abducens nucleus, and/or the medial longitudinal fasciculus produce various horizontal oculomotor deficits, including total conjugate lateral gaze palsy, unilateral or bilateral internuclear ophthalmoplegia, and one-and-a-half syndrome. 
The majority of stroke cases with conjugate gaze deviation are seen with cortical lesions affecting the frontal eye fields (FEF), as opposed to our case with a lesion of the anterior limb of the internal capsule. The internal capsule possesses highly conserved topography, with the genu containing the corticobulbar tract, and the posterior limb carrying corticospinal, corticorubral, and corticopontine tracts in addition to ascending sensory thalamocortical fibers. The anterior limb of the internal capsule contains predominantly front pontine tracts and thalamocortical fibers.
Diagnosis
History
A careful history is important to the diagnosis and patient should be specifically questioned on features of the etiologies described above.
Physical examination
For any type of ocular motor dysfunction, it is very important to have a systematic approach due to the complexity of the system involved including the ocular motor, vestibular, and cerebellar pathways. Key tests to consider are noted below:
- It is important to inspect the patient for any anomalous head position (e.g. chin up or chin down position) and to check for any gaze preferences or primary position deviations.
- Orthoptic evaluation of the function of the extraocular muscles in all nine cardinal positions of gaze should be examined for any vertical misalignment, deficits of duction or versions, and the presence or absence of nystagmus.
- The cover/uncover test and alternating cover tests may also be performed to assess for ocular alignment in the diagnostic positions of gaze and primary position.
- Saccade testing is performed by asking the patient to look back and forth quickly between two targets to check for latency, velocity, and conjugacy of the fast eye movements.
- Smooth pursuit is checked by having the patient visually track an object moving slowly in vertical direction while keeping the head stationary. If ocular movement fails to match the velocity of the moving object, a corrective saccade will occur. Because smooth pursuit involves many neural structures and may be affected by various factors, impaired smooth pursuit is typically non-localizing.
- Optokinetic nystagmus is checked by using an optokinetic drum, where both the smooth pursuit and saccades are tested at the same time. This test is useful in patients who cannot voluntarily initiate saccades.
- If passive rotation of the head by the examiner while the patient fixates on an object result in improved or full vertical ocular movements, this indicates a supranuclear cause (i.e., the doll’s eye maneuver).
Signs
Along with vertical gaze palsy (VGP), patients can have several other signs that help identify specific syndromes.
Parinaud/Dorsal Midbrain syndrome 
The full or partial Parinaud syndrome results from lesions (e.g., pineal gland tumors) of the dorsal midbrain. As noted previously, posterior commissure lesions typically lead to limitations of upward gaze and may be associated with a downward gaze preference (i.e., the ‘setting sun’ sign). Other signs of the dorsal midbrain syndrome include bilateral lid retraction (Collier sign), skew deviation, convergence retraction nystagmus, and pupillary abnormalities (light-near dissociation).
Niemann- Pick Disease Type C
This is a neurodegenerative disease caused by a genetic mutation in NPC1 (≥95% of cases) or NPC2 which leads to inflammations in arteries which leads to the defects in the intracellular lipid trafficking and an accumulation of cholesterol in peripheral organs and glycosphingolipids in the CNS causing cell dysfunction and death. The age at presentation for Niemann Pick disease is highly variable; however, age at neurologic symptom onset and type of symptoms are prognostic factors for disease severity and life expectancy. Early on in this disease due to cell damage or dysfunction in the riMLF, patients develop slow vertical saccades in a downward direction along with frequent blinking. Facial dystonia with facial grimacing in the presence of supranuclear gaze palsy is characteristic for Niemann-Pick Disease Type C. Vertical saccade paresis may be present prior to the systemic, neurological, or psychiatric signs and may be the only sign in adults suffering from this disease, thus warranting further workup.
Progressive Supranuclear Palsy
PSP is a neurodegenerative disease of unknown etiology in which neurons in the basal ganglia and brainstem degenerate. Clinical signs include downgaze palsy, loss of balance with backward falls, muscle rigidity, dysphagia, dysarthria, emotional lability (pseudobulbar palsy), mild dementia and resting tremor. A characteristic sign for PSP is the “round the houses” sign where vertical saccades follow a curved course due to inability to produce pure midline movement. Although Parkinson’s disease (PD) and PSP share several clinical features, downgaze palsy is not seen in PD and should lead clinicians to consider the diagnosis of PSP. The lesion is located above the cranial nerve nuclei that control vertical gaze, thus the name “supranuclear.”
Cortico-Basal Syndrome (CBS)
Cortico0-basal syndrome is a progressive neurodegenerative disease and is considered a parkinsonism-plus syndrome, an atypical form of parkinsonism. It shares clinical features with both PD and PSP; however, vertical gaze palsy in cortico-basal syndrome is typically delayed more than 3 years after symptom onset. Other clinical features include inability to initiate saccades to verbal commands despite retained spontaneous saccades, blepharospasm, and eyelid opening apraxia.
Symptoms
Symptoms include blurred vision, decrease in visual acuity with worsening while reading, oscillopsia (bouncing images) if nystagmus is present, along with dizziness, vertigo, postural imbalance, gait disturbances/ataxia, and increased risk of falls.
Diagnosis
Vertical gaze palsy (VGP) usually selectively affects saccades. Upgaze palsy is most common, then combined upgaze and downgaze followed by downgaze palsy. If the riMLF is affected, other signs include pupillary or ocular motor signs of third nerve palsies including wall-eyed bilateral internuclear ophthalmoplegia, impaired convergence, and skew deviation. If there is thalamic damage, behavioral disturbances can be noted such as hemineglect, akinetic mutism, or subcortical demented states with apathy and slowness of thought. If the posterior commissure is affected, pathologic lid retraction while looking straight ahead (Collier sign) can be present along with mid-dilated pupils that show a smaller reaction to light than to near stimulus stimulus (light-near dissociation). Attempted upward saccades producing a convergence-retraction nystagmus may also be present.
Diagnostic procedures
Neuroimaging (preferably magnetic resonance imaging of the brain with and without contrast) can help with both localization of the lesion and determination of etiology, especially if vascular or neoplastic in nature. If an infectious cause is suspected, consider serum and CSF testing for common chronic infections such as tuberculosis and syphilis. Whipple disease diagnosis requires special periodic acid-Schiff (PAS) stains of pathologic samples or PCR, typically obtained from the gastrointestinal tract or other affected tissues. In regard to metabolic conditions, such as Niemann-Pick type C, work-up may include serum transasminase evaluation, skin fibroblast assays for sphingomyelinase activity, and possibly genetic testing.
Differential diagnosis 
Infranuclear disorders such as myasthenia gravis (MG) and thyroid eye disease (TED) should be considered in the differential when ruling out vertical gaze palsy (VGP). In thyroid eye disease, bilateral inferior recti involvement can mimic up gaze palsy. In MG, any ocular muscle can be affected, coincidentally leading to a vertical gaze palsy (VGP) bilaterally. Both types of diseases, however, do not tend to be perfectly symmetric and MG should be variable over time. They can be diagnosed with lab testing (e.g. antithyroid and antiacetylcholine receptor antibodies), orbital ultrasound (for eye muscle enlargement in TED), and EMG (decremental response is seen in MG).
Allopathic treatment for gaze palsy
Allopathic treatments are to focus on symptom management. Management of supranuclear vertical gaze palsy (VGP) is directed at treatment of the underlying disease and symptomatic management ophthalmic complaints. For example, vascular etiologies such as stroke may be managed with antiplatelet or anticoagulant therapy. Niemann-Pick Disease Type C may have improved prognosis with miglustat. Studies demonstrate that miglustat may delay neurological deterioration and prolong survival in adults.
Levodopa treatment for Parkinson’s Disease may improve ophthalmic manifestations such as saccadic accuracy and smooth pursuit.
Surgical management may be indicated for neoplasms or refractory symptoms.
For diplopia and other ophthalmic complaints, treatments are typically conservative and may include refractive correction, a temporary Fresnel prism or ground-in prism glass.
Vision rehabilitation therapies in conjunction with physical and occupational therapy may also be of benefit. Single vision glasses and readers should be used in patients with downgaze palsy who cannot use a bifocal or progressive add lenses effectively.
Homeopathic Treatment for gaze palsy 
Homeopathic treatments are not to focus on only symptom but to treat the root cause along with the symptoms. Treatment of supranuclear vertical gaze palsy (VGP) is directed at treatment of the underlying disease and ophthalmic complaints. For example, vascular etiologies such as stroke could be treated with Homeopathic medicines. Niemann-Pick Disease Type C could be treated with Homeopathy. Homeopathic treatment for Parkinson’s Disease may cure ophthalmic manifestations such as saccadic accuracy and smooth pursuit.
Note: To shorten the article for your convenience, for each disease Homeopathic treatment please click the specific link given above.
Prognosis
The prognosis for vertical gaze palsy (VGP) depends on the underlying etiology and treatment type; in allopathy there is no complete cure for gaze palsy, on the other hand Homeopathy can easily handle and cure gaze palsy and its root causes (central nervous system {Stroke, Parkinson’s disease etc.}, Neiman Pick disease etc.) in 30-90 days.
If allopathic medication is provoking the symptoms, improvement may be seen after medication discontinuation (not sure). Similarly, allopathic treatment of a compressive lesion or lowering of elevated intracranial pressure may result in improvement. The condition can be permanent due to the irreversible nature of the lesion in many cases. Neurodegenerative disease (e.g., PSP) typically exhibits slow progression.
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