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|LETTERS TO EDITOR
|Year : 2019 | Volume
| Issue : 5 | Page : 1390-1392
A Case of Oculomotor Nerve Palsy caused by Neurovascular Compression by the Fetal Posterior Communicating Artery with a Review of Literature
Kulumani M Sivasubramaniyan1, Krishnan Nagarajan1, Aghoram Rajeswari2, Anbazhagan Sathiaprabhu3
1 Department of Radio-diagnosis, Jawaharlal Institute of Postgraduate Medical Education and Research, Pondicherry, India
2 Department of Neurology, Jawaharlal Institute of Postgraduate Medical Education and Research, Pondicherry, India
3 Department of Neurosurgery, Jawaharlal Institute of Postgraduate Medical Education and Research, Pondicherry, India
|Date of Web Publication||19-Nov-2019|
Dr. Krishnan Nagarajan
Department of Radio-diagnosis, Jawaharlal Institute of Postgraduate Medical Education and Research (JIPMER), Dhanvantri Nagar, Pondicherry - 605 006
Source of Support: None, Conflict of Interest: None
|How to cite this article:|
Sivasubramaniyan KM, Nagarajan K, Rajeswari A, Sathiaprabhu A. A Case of Oculomotor Nerve Palsy caused by Neurovascular Compression by the Fetal Posterior Communicating Artery with a Review of Literature. Neurol India 2019;67:1390-2
|How to cite this URL:|
Sivasubramaniyan KM, Nagarajan K, Rajeswari A, Sathiaprabhu A. A Case of Oculomotor Nerve Palsy caused by Neurovascular Compression by the Fetal Posterior Communicating Artery with a Review of Literature. Neurol India [serial online] 2019 [cited 2020 Aug 14];67:1390-2. Available from: http://www.neurologyindia.com/text.asp?2019/67/5/1390/271270
Isolated oculomotor nerve palsy (ONP) invariably comes to the attention of the radiologist for imaging evaluation of the brain to rule out structural causes. Apart from mass lesions in the midbrain, vascular causes along the course of the nerve such as aneurysms of the posterior communicating artery, neurovascular conflicts can occur along the cisternal portion of the oculomotornerve by adjacent normal vascular structures. With the advent of newer heavily T2-weighted magnetic resonance (MR) sequences that image cranial nerves such as three-dimensional (3D) constructive interference in steady state or fast imaging employing steady-state acquisition or 3D T2-SPACE and MR angiography (MRA), more and more cases of neurovascular conflicts are being reported. In an otherwise normal looking brain, the cranial nerve sequence might be the only aid in the diagnosis of neurovascular conflict. The common vessels found to cause oculomotor neurovascular conflict as reviewed in the literature are the posterior cerebral artery (PCA), superior cerebellar artery (SCA), posterior communicating (PCom) artery, tortuous internal carotid artery (ICA), and anatomical variants such as persistent trigeminal artery and duplicate or elongated SCA.
A 54-year-old, right-handed female health worker noticed a sudden-onset inability to open her right eye during the day while at work. Her co-workers noticed that she had altered visual axes. She also complained of right-sided headache and mild blurring of vision. There was no significant history of trauma or limb weakness. There was no history of diabetes mellitus, hypertension or tuberculosis. Her blood pressure at the time of presentation was 114/72 mm Hg. On examination, there was partial ptosis of the right eyelid. The left pupil was 3 mm in diameter and reacted normally to light stimulation. The right pupil was mydriatic (5 mm) and reacted poorly to testing for direct and consensual pupillary light reflexes. There was a loss of accommodation with the absence of convergence of the right eyeball. Elevation and adduction of the right eye was impaired. There was no visual impairment detected at the time of examination. The rest of the cranial nerve and neurological examination was normal. The patient's total blood count, erythrocyte sedimentation rate, random blood glucose, electrolytes, thyroid profile, and renal parameters were normal. Magnetic resonance imaging (MRI) of the brain was done and was unremarkable in routine T1-, T2-weighted, and FLAIR sequences. The MRA of the circle of Willis showed fetal origin of the right PCA arising from the right ICA. The P1 segment of the right PCA was hypoplastic [Figure 1]. On thin-section (1 mm) 3D T2-weighted Sampling Perfection with Application optimized Contrast using different flip-angle Evolutions (SPACE) imaging, the right oculomotor nerve was distorted and displaced inferomedially by the fetal PCA [Figure 2] and [Figure 3]. The patient was started on 100 mg of oral carbamazepine (Tegretol) twice daily. Over the next few days, the patient's ptosis, anisocoria, impaired pupillary light reflexes, and ophthalmoplegia started improving. She had resolution of her symptoms without any requirement of increasing the drug dose. She has been on follow-up for the past 9 months without any recurrence of symptoms.
|Figure 1: MR Angiogram (3D Time of Flight TOF) image (a) showing right-sided fetal type of posterior communicating (PCom) and posterior cerebral arteries (PCA). Coronal T2-weighted image (b) showing prominent right posterior communicating (PCom) artery in the suprasellar cistern|
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|Figure 2: 3D Heavily T2-weighted SPACE sequence in Coronal (a) and Axial (b) planes showing PCom (Arrow in a and star in b) indenting the 3rd nerve in the cistern|
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|Figure 3: 3D SPACE oblique sagittal reformations showing the exiting 3rd nerve from midbrain (a) and PCom coursing (b) close to each other|
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Neurovascular compression syndromes are usually caused by arteries that directly contact the cisternal portion of a cranial nerve. The transition zone (TZ) between the central and peripheral myelin is the most vulnerable region for symptomatic neurovascular compression. The TZ overlaps the root entry/exit zone (REZ) of most cranial nerves such as the trigeminal, facial, and glossopharyngeal nerves. Of the cranial nerves studied to date, the oculomotor nerve rootlets vary most markedly in size and TZ length. Hence, the variability of overlap between the TZ and the REZ of the oculomotor nerve is understudied and unpredictable. Because neurovascular contacts are seen in asymptomatic patients quite often, neurovascular conflict should be diagnosed only when nerve deviation or indentation is noted.
The criteria for neurovascular conflict state are as follows:
- The offending vessel must be an artery
- The site of contact must be the REZ
- The vessel must cross the nerve perpendicularly
- The nerve must be deviated or indented by the vessel or compressed or encased between two or more adjacent vessels in the appropriate clinical setting.
On emerging from the brain, the oculomotor nerve is invested in a sheath of pia mater and enclosed in a prolongation from the arachnoid. It passes between the SCA and PCA and then pierces the dura mater in front of and lateral to the posterior clinoid process passing between the free and the attached borders of the tentorium cerebelli. It runs along the lateral wall of the cavernous sinus above the other orbital nerves. Following the development of the vertebral artery in the fetus and the establishment of a typical adult posterior circulation if the PCom fails to regress and persist as the main supply to the PCA, it is termed as a fetal type PCom. It is a very common configuration. It may be unilateral or bilateral. The fetal configuration or origin of the PCA is further divided in to full fetal-type PCA (full FTP) and partial fetal-type PCA (partial FTP), as proposed by van Raamt et al. In full FTP the P1 segment may be absent, whereas in partial FTP there is some connection with the P1 but with caliber less than the ipsilateral PCom. The oculomotor nerve courses amidst several intracranial arteries along its cisternal segment and is prone to neurovascular conflict [Table 1].
|Table 1: Showing previous reports of non-aneurysmal vascular compression causes of the third nerve palsy|
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In 1973, Hopkins et al. published a case report of ONP in an 81-year-old female secondary to a tortuous feta-type PCA. Since then, three additional cases of fetal PCA causing ONP have been described., Liang et al. in their study of relation of oculomotor nerve and adjacent vascular structures observed that the PCA contacted the oculomotor nerve in 216 (55.1%) of 392 nerves, and the SCA was observed to contact the oculomotor nerve in 231 (58.9%) of 392 nerves. The abnormal nerve compression in nine patients with paralysis of oculomotor nerve was displayed well in all patients. Wang et al. used MRI in asymptomatic patients and differentiated three levels of nerve-vessel contact and reported that the cisternal segment of the oculomotor nerve did not have contact with any artery (level 1) in 27.4% (51/186 nerves); one hundred nerves made contact with at least one artery (level 2), but their shapes or configurations were not changed; 35 nerves (18.8%) were displaced or distorted because of artery compression (level 3). The PCA had the greatest incidence of making contact with or compressing the cisternal segment of the oculomotor nerve (58.1%).
Joshi et al. demonstrated neurovascular compression of cisternal oculomotor nerve as it curved over a duplicated SCA on high-resolution MRI in a patient with transient ONP. Trechot et al. demonstrated vascular and osteodural compression of the oculomotor nerve between a tortuous PCoA and posterior clinoid process at the entrance of cavernous sinus. Tan et al. described ONP caused by neurovascular compression by an aberrant PCA of basilar origin (nonfetal PCA).
Few other case reports of complete ONP have been described owing to direct compression by the posterior cerebral artery, intraoperatively confirmed vessel loop compression at the exit zone of the oculomotor nerve from the midbrain, vascular compression by PCom,, persistent trigeminal artery, and an elongated SCA.
A heavily T2-weighted 3D SPACE for imaging the cranial nerves and a TOF-MRA are important sequences and are indispensable for diagnosing neurovascular conflict. Before concluding that acquired ONP is idiopathic, it is important to rule out neurovascular conflict by MR imaging. The knowledge of anatomical variants of the circle of Willis is absolutely essential in relating to the potential causes of oculomotor neurovascular conflict.
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[Figure 1], [Figure 2], [Figure 3]