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    Top 5 neuro signs never to ignore


    The third nerve palsy can be partial or complete based on the extent of the lesion and the pupil may or may not be involved.17 In a third nerve palsy, the anisocoria is greater in the light and is characterized by a dilated and poorly reactive or non-reactive pupil on the ipsilateral side.

    This anisocoria is key in differentiating between ischemic and compressive causes of complete third nerve palsy. The parasympathetic fibers travel along the superficial surface of the oculomotor nerve to innervate the ciliary muscle, which makes them more susceptible to a compressive injury vs. the internally located motor fibers.17,18

    The most worrisome compressive lesion causing a third nerve palsy is an aneurysm of the posterior communicating artery (PCOM).3,18 A neurologically isolated, painless, complete third nerve palsy without pupil involvement in a vasculopathic patient is generally at low risk for a compressive lesion and is more likely to be ischemic.3,18 However, a small percentage of PCOM aneurysms present with normal pupils initially, especially in partial third nerve palsies, and therefore neuroimaging and further work up may still be necessary.18

    In an acute setting, a CT with CTA of the brain is the recommended first line imaging.3,18,19 A contrast CTA should be able to detect an aneurysm as small as 3 mm.20,21 If the CTA is negative, then the next line of testing is an MRI of brain and orbits with and without contrast and MRA.3,18

    Despite the high combined sensitivities of CTA with MRI and MRA, standard catheter angiogram remains the gold standard depending on the index of suspicion for aneurysm.3

    The prognosis of the third nerve palsy depends on the etiology. In cases of aneurysmal compression, improvement is generally seen following surgical or endovascular treatment. Third nerve palsies secondary to ischemia typically improve over four to 12 weeks.

    5. Acute painful anisocoria greater in the dark

    A 35-year-old male presents with new onset headache and anisocoria after playing basketball. A right sided 2 mm ptosis, upside-down ptosis, and ipsilateral miosis was also present. The anisocoria was greater in the dark with a dilation lag of the pupil OD. The rest of the eye exam was normal.

    Acute painful ptosis and miosis should be considered as an ipsilateral internal carotid dissection from damage to the oculosympathetic pathway producing a Horner syndrome (HS). Other causes for the HS include malignancy, stroke, and aneurysm.

    Damage along any point of the oculosympathetic pathway can produce a HS. The first order neuron begins in the hypothalamus and descends posterolaterally in the brainstem to synapse in the ciliospinal center of budge at the level of C8-T2. This second order neuron then exits the spinal cord and travels over lung apex (Pancoast lung tumor) to synapse within the superior cervical ganglion at the bifurcation of the common carotid artery. The third order neuron ascends through the cavernous sinus via the adventitia of the internal carotid artery before traveling a short course on the abducens nerve and joining the first division of the trigeminal nerve where it travels through the superior orbital fissure to innervate the Mullers muscle and iris dilator.3

    Pharmacologic testing is often helpful in confirming the diagnosis, but neuroimaging is recommended for all patients with a suspected HS clinically.


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