0

20 30s

proximal myopathy

feeling Fine at end of dey Feeling weak

pf wakeup

113rescue spoutons 143 become worse 143 died



female

Bimodel distributors 2e Sos

60 70s male

i chalinestrase inubiton

2 steroid

3 Thymeetsmy

cholinesterase inhibitors

CLINICAL APPROACH TO PTOSIS

— The history and physical examination can identify the cause of ptosis in most patients . Additional
diagnostic tests are indicated in some patients.

History — The historical features center on the timing and associated symptoms of the ptosis.
Important information to gather includes the following:

●Has it been present from birth?

●Was this acute or slowly progressive?

●Does the degree of ptosis vary over the course of the day or with fatigue?

●Is there any associated headache or diplopia?

●Is there a history of ocular surgery, trauma (including birth trauma), or contact lens wear?

●Is there a family history of ptosis?

It may be helpful to consult family members and review old photographs to understand the duration
and progression of the condition.

Examination — A number of examination features may help determine the cause of ptosis (table 1). The
examination begins with noting head posture and eyebrow position. Patients with ptosis may assume a
chin up position to look through the lowered palpebral fissure. The eyebrows may be elevated in an
effort to raise the lids. Next, the eyelid position should be noted with the patient at rest with the
eyebrows relaxed and the eyes in primary gaze. Anatomic landmarks: eyelid crease, palpebral fissure
(PF) and margin reflex distance (MRD) should be specifically noted (see 'Landmarks' above). The PF
might increase in downgaze in congenital ptosis but generally decreases in downgaze in acquired
causes of ptosis.

Hering's law of equal innervation applies to eyelid muscles, which are innervated by a single midline
brainstem nucleus providing equal bilateral central output. In unilateral ptosis, excessive innervational
stimulation often causes the contralateral eyelid to appear retracted (picture 2). If ptosis is bilateral but
asymmetric, the less affected eyelid may appear normal. This can sometimes be detected by manual
elevation of the obviously ptotic eyelid; a fall of the contralateral eyelid or "curtaining" confirms the
bilaterality of the condition.

Levator function (LF) is assessed by measuring the excursion of the eyelid margin from downgaze to
upgaze. Stabilizing the eyebrow to avoid overestimating the excursion of the lid margin may be
accomplished by gentle fingertip pressure on the brow (picture 3). Normal LF is greater than 12 mm [4].
Horner syndrome causes ptosis by reducing activity of Müller's muscle; LF remains intact. LF is also
preserved in acquired aponeurotic ptosis. Myopathic, congenital, and neuromuscular junction causes
of ptosis have reduced LF.

With the patient looking downward, the physician can measure the distance from the eyelid crease to
the eyelid margin (normal approximately 6.5 mm) [5]. An increased distance or redundancy of the eyelid
crease suggests levator aponeurosis dehiscence or slippage [6]. This crease is not appreciable in most
Asian eyelids [3]. The crease is often less distinct or absent in patients with congenital ptosis.

The examination should also include notation of pupil size and reactivity. When a third nerve palsy
involves the pupil, it will appear larger than the contralateral pupil and react poorly to light and
accommodation. In contrast, an ipsilateral, miotic pupil with normal reactivity will accompany ptosis in
the setting of a Horner syndrome. The anisocoria is more evident in a darkened room.

Extraocular motility and ocular alignment should be tested. Lesions of the third cranial nerve will
frequently include some eye movement abnormality (see 'Third nerve palsy' below). Orbicularis
weakness suggests a myopathic or neuromuscular junction cause. Myopathic disease often results in
bilateral symmetric ophthalmoplegia without diplopia. Eye movements may be normal or abnormal in
cases of myasthenia gravis.

Evidence of levator fatigue should be sought for the diagnosis of neuromuscular junction disease. If the
ptosis fluctuates throughout the examination, then evidence for fatigability of the levator muscle is
present. Fatigue can also be induced by prolonged activation of the levator palpebrae muscle in
sustained upgaze for one to two minutes [7]. Enhancement of ptosis during prolonged upgaze or upon
return to primary gaze suggests fatigability. Eyelid "curtaining" as discussed above is suggestive but
not specific for fatigability. Finally, a Cogan lid twitch, a transient overshoot of eyelid position when
patient saccades from downgaze to primary gaze position also suggests eyelid fatigability.