Clinical History

Because cranial nerves III, IV, and VI innervate the extraocular muscles that move the eyes, the striated muscles that elevate the upper eyelids, and the iris sphincters that constrict the pupils, several symptoms develop when damage occurs. In general, dysfunction of these nerves causes different combinations of binocular double vision from misalignment of the visual axes. Damage to cranial nerve III causes ptosis from weakness of the levator palpebrae muscle, as well as pupil mydriasis or dilatation from paresis of the iris sphincter muscle.

Altered function in the supranuclear control of the ocular motor system leads to conjugate gaze palsy or paresis in which the visual axes remain parallel or appropriately convergent on the object of regard. In these settings, the patient does not experience diplopia, because the two eyes simultaneously fail to achieve full movement in one or several directions from primary gaze. In some cases of conjugate gaze paresis, the eyes fail to deviate fully into the defective direction, and in other cases, the deficit is more subtle, so that the eyes deviate fully but move more slowly than they should or with an interrupted course. These dynamic alterations are generally without subjective symptoms and must be observed during the course of examination. Even patients with complete lack of gaze in a particular direction often have no complaints but automatically turn their head to compensate for the loss of eye deviation. The major exception to this principle is loss of downgaze, which generally creates much difficulty for the patient even when walking on a flat surface and especially in negotiating stairs and other uneven terrain. This is particularly irksome when coupled with the involuntary head and neck retraction or extension that often accompanies progressive supranuclear palsy (PSP) (see Cha.pter.34 ). Falling backward is common in PSP patients, and this problem should also be asked about specifically. A key symptom of pathological underactivity in the vestibulo-ocular reflex is oscillopsia, which is an illusory sense of movement of the visual environment as the head moves. This is a direct consequence of foveal image slippage engendered specifically by head movement, and the illusion ceases when the head is immobile. Vertigo, another common symptom of vestibular disorders, is often present when the head is still, although it is usually aggravated by

head movement. Vertigo is a rotational illusion that is often accompanied by rhythmical oscillopsia as a consequence of nystagmus, in which case the rhythm is imposed by the regular fast phases of the nystagmus. The vertigo may be subjective, in which case patients feel as though they are rotating, or it may be objective, in which case they perceive that the environment is rotating.

The time course of the symptoms constitutes the best evidence for the etiology of the disorder and must be probed in detail. Diplopia is a markedly troublesome symptom, and it is either present or not, making its onset always acute. The angle of deviation between the eyes and the consequent distance between the two images may vary after onset, and this feature can be used to discern whether the course is stationary, progressive, or remitting. Symptoms from compressive cranial nerve lesions secondary to tumors and from degenerative conditions generally have a progressive course, whereas inflammatory diseases such as orbital inflammatory pseudotumor or Tolosa-Hunt syndrome (orbital and cavernous sinus inflammation, respectively) (see C.hap.ter.53 ) often run either a course of remissions and exacerbations or a progressive course. Ischemic causes tend to produce a stationary or, more commonly, a remitting course.

Both ischemic and inflammatory disorders of cranial nerves III, IV, or VI tend to be associated with pain in the ipsilateral eye or orbit, sometimes with wide radiation to the brow, frontal, and temporal regions and downward into the cheek and even to the mandible. Malignant neoplasms may involve the cranial nerves III, IV, and VI anywhere along their courses, and pain can accompany the other features, especially when there is meningeal, bony, or dural infiltration. As with inflammatory diseases, the pain is usually centered on the ipsilateral orbit but may radiate widely. Not infrequently, intraorbital lesions, even malignant ones, can involve the cranial nerves without pain, possibly because they do not stretch or invade pain-sensitive structures, including muscle and particularly dura and periosteum. Absence of pain, therefore, should not in itself engender a false sense of security that the lesion causing the cranial neuropathy is benign.

A detailed characterization of the direction and circumstances of image separation is important in establishing which muscle or muscles, and hence, which cranial nerve or nerves, are involved. Horizontal diplopia arises from disorders affecting either the lateral rectus or medial rectus muscles. If the paretic muscle is one or both lateral rectus pair, the visual axes will be convergent (esotropia), and if the involved muscle is one or both medial recti, the visual axes will be divergent (exotropia). It is important to note that at minimal angles of binocular divergence, the patient often describes the visual experience as a blur rather than doubling of images. It is important to ask any patient with blurred vision if it clears on covering either eye, which will be the case for blur that is a result of minimal angle binocular diplopia. Blurring can be misconstrued for diminished acuity, but acuity is a function of cranial nerve II. Patients often cannot tell from the diplopia whether they have convergent or divergent eyes, because either condition produces horizontal image separation. Asking the patient when he or she covers the right eye whether the right or left image disappears can be helpful. If the eyes are exodeviated (divergent), the image to the left disappears. If the eyes are esodeviated (convergent), the image to the right disappears. A convenient way to remember the directions is to consider that crossed (X) diplopia results from eXodeviation (divergent visual axes, medial rectus weakness) and homonymous, or same side, diplopia results from esodeviation (convergent visual axes, lateral rectus weakness). The terms crossed and homonymous refer to the relation between the side of the eye covered and the relative position of the image that disappears--on the same (homonymous) or opposite (crossed) side. This same principle underlies diplopia testing and is considered in the examination section.

The visual axes are nearly parallel for viewing very distant objects. As the object of regard is brought progressively closer to the viewing subject, the person's visual axes must become more convergent to keep the images on both retinal foveas. Convergence is, therefore, a normal voluntary action in which the medial recti of both eyes are simultaneously activated and the resulting esodeviation is appropriate for near viewing. Because of this, patients with lateral rectus (sixth cranial nerve) dysfunction and esotropia have diplopia only for relatively distant objects. All objects in near space can be fused by adding normal convergence to the esotropia that results from the muscle weakness. On the other hand, patients with exotropia do not have single vision at any distance. The presence or absence of fusion and single vision at some near point can be used to discern esotropia from exotropia.

Vertical image separation implies dysfunction of a vertically acting muscle in one or both eyes. These include the superior rectus and oblique and the inferior rectus and oblique muscles on either side. The details of image separation for vertical muscle imbalance must usually await examination using diplopia testing, but the patient may be able to supply some useful hints by way of history. Patients with a third cranial nerve dysfunction usually have mixed horizontal and vertical diplopia (oblique image separation) because several vertical muscles and the horizontally acting medial rectus muscle are commonly involved together. Also, these patients usually have some degree of upper eyelid ptosis, which is noticed by the patient on looking in the mirror. As ptosis becomes more severe, there is first restriction of the upper visual field and then loss of all vision when the pupil is completely covered. Asking the patient about upper field loss and total vision loss can help plot the time course of the ptosis. The most common neural cause of isolated vertical diplopia is fourth cranial nerve dysfunction. The weak muscle is the superior oblique, which turns the eye down (depression) and does so most efficiently in adduction (horizontal deviation toward the nose). The image separation is widest in downgaze and looking to the side opposite the lesion, which brings the involved eye into adduction. If the patient can say that the vertical diplopia is wider looking down and widest looking down and to the left, then right superior oblique muscle weakness is most likely and vice versa. The diplopia is isolated in fourth cranial nerve palsy because the nerve does not innervate any muscles other than the superior oblique and, in that respect, differs from third cranial nerve palsy, with its multiplicity of simultaneously involved muscles.

Patients with fourth cranial nerve palsy often have torsional imbalance with excyclodeviation of the involved eye. Most patients automatically compensate by tilting and turning the head to minimize and sometimes eliminate diplopia. The resulting head position--tucked down, turned away, and tilted away--is characteristic and usually has been noticed as peculiar by others if not by the patient himself or herself. Patients often avoid diplopia altogether by using the compensatory head position. It can be useful to ask when people started saying things about the patient's head position, if it is unclear when the fourth nerve palsy really started. Also, it is useful to review family photographs from the patient's childhood and infancy. Head tilt in a childhood photo is good evidence of congenital fourth cranial nerve palsy--a common condition that may present with the onset of diplopia later in life.

Oculomotor dysfunction may occur in the setting of any systemic disorder. One of the most common diseases to affect ocular motility is thyroid orbitopathy. The past history is particularly important because thyroid function studies are commonly normal when the patients present with orbital findings. A history of fatigue, weight change, skin alterations, heat intolerance, and other constitutional symptoms is thus important to elicit. A large contingent of patients who present with cranial mononeuropathies have a presumed ischemic etiology based on putative small vessel occlusive disease. These can usually present in persons older than 60 years of age, and many have other arteriosclerotic risk factors such as systemic hypertension or diabetes mellitus. A history of these disorders should be elicited by the interviewer. A full inquiry about multisystem signs and symptoms is essential to identify collagen vascular diseases such as periarteritis nodosa or systemic lupus erythematosus, which may be complicated by ischemic cranial mononeuropathy. Orbital inflammatory pseudotumor or Tolosa-Hunt syndrome may be caused by sarcoidosis, and the history should be probed for any of its many systemic manifestations including skin, muscle, joint, pulmonary, hepatic, or renal involvement. Myasthenia gravis frequently presents with ptosis and weakness of various extraocular muscles and may closely mimic cranial nerve lesions. This neuromuscular disorder (see Chapter SO ) has the remarkable capacity to look like a pupil-sparing third cranial nerve palsy or, in a more limited case, internuclear ophthalmoplegia (INO) from a lesion along the medial longitudinal fasciculus (MLF) in the brain stem. [ii Myasthenia most frequently runs a remitting, exacerbating course with involvement of axial and appendicular muscle groups. It is important, therefore, to ask about past or concurrent weakness in the limbs, trouble swallowing, weak phonation, and trouble breathing. Finally, a full family history and review of all medications is necessary. Many commonly prescribed general medical and neurological drugs can be associated with diplopia (carbamazepine, phenytoin), particularly at toxic levels.


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