Gaze holding helps to maintain eye in the eccentric eye position.
This is done with the help of the Pulse-step innervation
When the eye moves towards the corner and if the neural integrator is
perfect the viscous drag is overcome by the pulse and made to stay in the
extremes of gaze by the step.
And if the neural integrator is leaky eye moves and from there due to
leaky potential it moves
towards the central.
What are
the causes of Gaze evoked nystagmus ?
1. Due to
leaky neural integrator
Lesion of Nucleus prepositus hypoglossi/ Medial Vestibular Nuclei
Horizontal gaze evoked nystagmus
Direction changing nystagmus
Fast component is the direction of fixation
Bilateral lesion of INC
Impaired vertical gaze holding
2. Lesions
of vestibulo-cerebellum
What are the types of Gaze evoked nystagmus?
Symmetrical gaze evoked nystagmus
Anticonvulsants, particularly phenytoin and phenobarbitone, and
ingestion of psychotropic drugs and alcohol.
In Joffroy's sign there is a lack of wrinkling of the forehead when a patient looks up with the head bent forwards Joffroys sign is a sign of hyperthyroidism.It is elicited as follows
Von Graefes sign is an important eye sign in hyperthyroidism.It is elicited as follows
The patient looks straight ahead.
Ask the patient to look down.
Look for a lag of the upper eyelid.
It is the lagging of the
upper eyelid on downward rotation of the eye and indicate underlying Graves' Disease
The
terms lid lag and von Graefe's sign have been used interchangeably in the past;
but, they are distinct signs of downgaze-related upper eyelid static position
and dynamic movement, respectively.
Rowland Payne syndrome - Consists of Horner's syndrome, phrenic nerve and recurrent laryngeal nerve involvement. It is caused in metastatic tumor at neck from malignancy like carcinoma breast.
Old age.
Argyll Robertson pupil.
Application of pilocarpine drops : overdose of neostigmine.
Iritis.
Bilateral miosis causes
Pin-point pupil.
Morphine or barbiturate poisoning,
heat stroke (hyperpyrexia)
How to differentiate between patients with pin point pupil
Pontine haemorrhage—There is coma, hyperpyrexia and long tract signs (ie. sings ol pyramidal tract lesion).
Organophosphorus poisoning— It is diagnosed by history, absense of long tract signs, and sign of respiratory depression. The patient may be unconscious but there is absense of pyrexia.
Mydriasis is defined as Pupil size > 5 mm
Constrictors ol the pupil are supplied by parasympathetics via the oculomotor nerve while the dilator are controlled by sympathetic nervous system. Changes in the size of the pupil do not affect the vision
Unilateral mydriasis causes
Drugs—-anticholinergics-
Acute ciliary ganglionitis—following several days after infection/ trauma
3rd nerve palsy.
Holmes-Adies pupil or myotonic pupil.
Blindness due to Optic atrophy
Acute congestive glaucoma.
Head injury-Uncal herniation Unilateral pupillary dilatation is the most important physical sign in the unconscious patient, and until proved otherwise a dilated pupil indicates that a herniated temporal lobe is compressing-the ipsilatcral oculomotor nerve, and that immediate surgical action is required.
Bilateral mydriasis causes
Anxiety
Myopic eyes
Infancy
Thyrotoxicosis
Drug poisoning-antihistamine, phenolhiazinc, anticholinergics, Datura poisoning,Drugs like atropine and pethidine
Normal size of pupil varies from 3 to 5 mm.
Pupils < 3mm size in average condition of illumination are called miotic and pupils > 5 mm are called mydriatic. Pin point pupil is said to be present when the pupillary size is less than or equal to 1 mm.
Normal—3-5 mm
Mydriasis > 6 mm
Miosis < 2 mm
Pin point pupil < I mm
A difference of 0.5 mm between the two pupils is abnormal
The 3rd cranial nerve-oculomotornerve
The oculomotor nuclear complex is located in the the middbrain at the level of superior colliculus. This has one unpaired and four paired nuclear columns.
The unpaired column constitute
Edinger-Westphal nucleus
Subnucleus for levator palpebrae superioris.
The paired nuclei constitutes
Subnuclei for superior, inferior and medial recti and inferior oblique.
4th cranial nerve-Trochlear nerve
Trochlear nerve passes posteriorly and the fibres from the right and left trochlear nuclei decussate on the dorsum of mid brain.
This is the only cranial nerve that emerges dorsally from the brainstem.
The left trochlear nucleus sends fibres to the right superior oblique muscle and vice versa.
6th cranial nerve-Abducent nerve
Abducent nerve has a very long intracranial course and supplies the lateral rectus muscle..
Because of its long intracranial course, this nerve is affected in conditions producing raised intracranial tension, hence producing a false localizing sign.
Rapid involuntary conjugate saccadic movement of eyes
It is described as rapid, involuntary, multivectorial (horizontal and vertical), unpredictable, conjugate fast eye movements without intersaccadic [quick rotation of the eyes] intervals) Ocular myoclonus associations
Opsoclonus Myoclonus Syndrome (OMS) is also called as Opsoclonus-Myoclonus-Ataxia (OMA), is a rare neurological disorder which appears to be the result of an autoimmune process involving the nervous system
Seen in Postencephalitic syndrome
Neuroblastoma
It may be seen associated with viral infection ,perhaps St. Louis encephalitis, Epstein-Barr, Coxsackie B, enterovirus, or just a flu
OPM-palatal myoclonus when associated with abnormal eye movements,it is called "oculopalatal myoclonus", or OPM. A clicking sound is commonly heard in this symptom
Anisocoria is the term used to describe the unequality in the size of the pupil.
The size of the pupil is controlled by muscles in the iris – the iris dilator and the iris constrictor muscles.
These muscles are controlled by nerves from the brain to the eye.
Any problems with these nerves rsults in the size of the pupil to be abnormal.
A problem with the nerve that normally dilates the pupil in the dark, causes a small pupil.
A problem with the nerve that normally constricts the pupil, produces an abnormally large pupil. Size of pupil is determined by the following factors
The size of the pupil is determined by the antagonistic action of thebsphincter constrictor muscle vs the diffuse dilator pupillae
Parasympathetic vs Sympathetic innervation
Local factors may alter this
How to elicit anisocoria?
• Ask the patient to gaze at lighted window or at some other distant light source so as to
see the pupil size.
• Look for unequal pupil, associated ptosis squint, reaction to light, to detect which side is normal. Causes of anisocoria
1.Unilateral sympathetic paralysis ? irritation
2.Unilateral 3rd nerve lesion as in
Brainstem damage
Transtentorial herniation
Pressure effect on 3rd nerve in tumors and aneurysm.
3. Commonest cause of anisocoria unequal pupils is the application of mydriatic to one eye.
.
Nystagmus is the
rhythmic, involuntary and jerky movements (oscillations) of the eyeball
when they are fixed on an object. Nystagmus signifies the disturbance in ocular
posture.
How to test for nystagmus?
At first,you should test the power of the extraocular muscles to
eliminate their weakness or paralysis because in such that situation,
nystagmoid movements will appear.
Now ask the patient to look forward. Observe for pendular
nystagmus
Fix the head of the patient with the left hand of the
examiner
Ask the patient to look at the examiner’s finger kept at 60
cm away from the patient.
Now the patient Is asked to fix his vision towards your
Index finger which is kept laterally to the
right side and then to the left side in turn (your finger
must be placed within the binocular vision
of the patient The
finger should he in the field of binocular vision, means not > 30° from
primary position or the medial limhus of the opposite eye should not cross the
punctum of the eyelid on that side.
Keep it for 5 seconds to detect latent nystagmus. It is
the examination of nystagmus in the horizontal plane.
Next place your
finger above and then below his head to examine the nystagmus in the vertical plane.
Strabismus or squint is tested by cover test or redglass test Red Glass Test
To identify the defective eye in diplopia
Patient is asked to look at an object placed in the direction of diplopia
Red glass is placed over one eye
A Red image is false if the eye over which the glass is placed is defective
A white image is false- the other eye is defective.
Principles
The outer image is the false image
The separation of the images is maximum in the direction of action of the paretic muscle Cover test
Instruct to fix the eyes on an object in front
Suddenly cover the apparently fixing eye, so that the other eye fixes
A deviation of the uncovered eye is called primary deviation
A deviation of the covered eye is called secondary deviation
Concomitant squint -primary deviation secondary deviation
Paralytic squint primary -deviation less than secondary deviation
1.Lateral gaze center is Frontal eyefield (FEF)
Lateral gaze center is Frontal eyefield (FEF) that is situated in area 8 the fibers descend through the internal capsule crosses to opposite side reaches brainstem the para-abducent nucleus of pons through abducent nerve reaches the lateral rectus to opposite side.
From para-abducent nucleus which is the pontine lateral gaze center fibers passes through medial longitudinal fasciculus (MLF) to the medial rectus nucleus of same side.
Stimulation of FEF result in conjugate gaze to opposite side.
Paralytic or destructive lesion of FEF result in Lateral gaze palsy to opposite side. Both eyes turn to same side.
Frontal eye field also controls saccadic movement to opposite side
Both eye field control vertical saccadic movement. This has regulatory effects on LPS. Stimulation of contraction of LPS resulting in opening of eye and dilatation of pupil. 2.Occipital gaze center area 18-19
Occipital gaze center area 18-19 cortico-fugal fibers passes through the optic radiation - post, limb of internal capsule - cerebral peduncle to 3rd nucleus and MLF.
Occipital gaze center control the pursuit movement occipital gaze center of one side control pursuit movement to the opposite side and same side.
Both occipital gaze centers together control vertical pursuit movement 3.Interstitial nucleus of cajal
It is situated at the level of Superior Colliculus it control the vertical gaze 4.Central nucleus of perlia is situated in the mid-brain is the center for convergence 5.Pontine lateral gaze center is close to 6th cranial nerve nuclei, send impulses to ipsilateral lateral rectus nuclei and contralateral Medial rectus nuclei through MLF
Stimulation produce lateral gaze to same side
Destruction produce lateral gaze to opposite side.
Introduction
INO is due to a lesion along the horizontal gaze pathway. This is one of the most localizing brainstem syndromes, resulting from a lesion in the medial longitudinal fasciculus (MLF) in the dorsomedial brainstem tegmentum of either the pons or the midbrain
Internuclear ophthalmoplegia (INO) is a disorder of conjugate lateral gaze in which the affected eye shows impairment of adduction. When an attempt is made to gaze contralaterally (relative to the affected eye), the affected eye adducts minimally, if at all. The contralateral eye abducts, however with nystagmus. Additionally, the divergence of the eyes leads to horizontal diplopia. So if the right eye is affected the patient will "see double" when looking to the left, seeing two images side-by-side. Converge.
The side of the INO is named by the side of the adduction deficit, which is ipsilateral to the medial longitudinal fasciculus (MLF) lesion. Types of INO
There are two types of INO that is Cogan's anterior and posterior INO, which refer to an anterior midbrain or posterior pontine localization along the medial longitudinal fasciculus (MLF). Symptoms and signs of INO Diplopia in INO
Patients with internuclear ophthalmoplegia (INO) may complain of horizontal diplopia when there is a significant adduction weakness or limitation on lateral gaze
Diplopia is not usually present in primary gaze.
Diplopia is due to the dysconjugate movement of the two eyes during horizontal gaze results in an interruption in binocular fusion that can lead to visual confusion, oscillopsia, diplopia, reading fatigue, and loss of stereopsis (depth perception) [ Vertigo in INO
Some patients also complain of vertigo The components of INO are
Impaired horizontal eye movement with weak adduction of the affected eye
Abduction nystagmus of the contralateral eye.
Convergence is generally preserved in INO
Adduction weakness in INO
Depending on the severity of the lesion, adduction of the involved eye may be impaired or absent. In milder cases, the deficit may be limited to a decrease in adduction velocity without ocular limitation of ocular movement
Milder forms of INO may be best elicited by asking the patient to perform fast horizontal eye movements (saccades) away from a fixed central point. Due to the Interruption of the ascending axons that arise from the internuclear neurons in the abducens nucleus likely explains the adduction deficit Abduction nystagmus in INO
The contralateral abducting eye will usually exhibit a disassociated horizontal nystagmus, although this does not always occur.
The underlying mechanisms causing abducting nystagmus are unknown. There is evidence that more than one mechanism may play a role in different patients and even in the same patient
One theory is that abduction nystagmus is due to an adaptive response to overcome the weakness of the contralateral medial rectus. This is explained by Hering's law of equal innervation, which states that attempts to increase innervation to the weak muscle in one eye are accompanied by a commensurate increase in innervation to the yoke muscle in the other eye.
Alternatively, gaze-evoked nystagmus may occur in patients with INO because of involvement of adjacent structures, such as the vestibular nuclei . The nystagmus is dissociated because adductor weakness limits its manifestation in the affected eye. Subclinical nystagmus in the adducting eye has been demonstrated with electro-ocular techniques Normal convergence in INO
Most lesions of the medial longitudinal fasciculus (MLF) are located in the pons or caudal mesencephalonhence they spare the vergence pathways, including the fibers deriving from the medial rectus subnucleus of cranial nerve III . As a result, convergence is intact in the most of the affected patients inspite of the adduction weakness on lateral gaze. Thisis an important finding that finding can be used to distinguish an INO from a partial third nerve palsy Abduction slowing
INO may produce slowing of abduction as well as adduction in the affected eye .This small degree of abduction slowing is expected in the context of adduction weakness, due to the loss of the contribution of the off-pulse of innervation (defective relaxation) when the medial rectus acts as an antagonist . Abnormal vertical eye movements in INO
As the MLF also contains pathways involved in the regulation of vertical pursuit, vertical vestibular signals, and vertical alignment , Patients often exhibit abnormalities with vertical eye movements, including:
Bobbing is also noticed in a patient with acute cerebellar hemorrhage without intrapontine challenging the myth that this sign is specific for intrapontine destruction
Clinical significance
Clinical significance of this sign bobbing is considered as a release phenomena and extremely poor prognostic sign for neurologic recovery.
Differential diagnosis
An initially fast upward deviation followed by a slow return to primary position is referred to as reverse ocular bobbing;
A slow initial upward drift followed by a fast return to primary position has been termed converse bobbing, or reverse ocular dipping.
Ocular bobbing has valuable localizing value and prognostic information
But, inverse bobbing, reverse bobbing, and dipping are nonlocalizing and most often noted with hypoxic-ischemic encephalopathy.
Pretectal pseudobobbing
It has been described with acute hydrocephalus.
This is an arrhythmic, repetitive downward and inward (V pattern) eye movements at a rate ranging from 1 per 3 seconds to 2 per second and an amplitude of 1/5 to 1/2 of the full voluntary range.
These movements may be mistaken for ocular bobbing, but their V pattern, their faster rate, and their pretectal rather than pontine-associated signs distinguished them from true pontine bobbing.
may have abnormal pupillary light reactions, intact horizontal eye movements, openand often retracted eyelids, a blink frequently preceding each eye movement, and a mute or stuporous rather than a comatose state.
