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Table of Contents    
Year : 2015  |  Volume : 63  |  Issue : 2  |  Page : 264-266

Bilateral ptosis after burr hole evacuation of a chronic subdural hematoma

1 Department of Neurosurgery, MS Ramaiah Medical College, Bangalore, Karnataka, India
2 Department of Neurosurgery, Consultant Neurosurgeon, `RLJ - MSR Neurocenter, Tamaka, Kolar, Karnataka, India
3 Department of Neuroanaesthesia, National Institute of Mental Health and Neurosciences, Bangalore, Karnataka, India

Date of Web Publication5-May-2015

Correspondence Address:
Krishna Chaitanya Joshi
Department of Neurosurgery, MS Ramaiah Medical College, Bangalore, Karnataka
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Source of Support: None, Conflict of Interest: None

DOI: 10.4103/0028-3886.156302

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How to cite this article:
Joshi KC, Murty P, Garg D, Varma RG. Bilateral ptosis after burr hole evacuation of a chronic subdural hematoma. Neurol India 2015;63:264-6

How to cite this URL:
Joshi KC, Murty P, Garg D, Varma RG. Bilateral ptosis after burr hole evacuation of a chronic subdural hematoma. Neurol India [serial online] 2015 [cited 2020 Nov 25];63:264-6. Available from:


The midline unpaired caudal nucleus of the third nerve lies in the midbrain, and supplies both the levators. Destructive lesions in this area or in the periaqueductal gray matter can lead to an isolated occurrence of bilateral ptosis. We present a unique case of a remote site hematoma in the midbrain following burr hole evacuation of a chronic subdural hematoma (CSDH) that caused bilateral ptosis.

A 55-year-old man presented to our emergency department with a history of progressive weakness of the right upper and lower limb, aphasia, increased somnolence, and headache since the last 3 days. He was a known alcoholic for the past 30 years. The relatives recollected that the patient had a trivial fall a month ago and sustained a minor injury to the head.

His computed tomography (CT) revealed a left-sided, fronto-temporo-parietal CSDH, with a moderate midline shift [Figure 1]. The routine preoperative hematological and biochemical parameters were normal. We performed a frontal and parietal burr hole drainage under general anesthesia. Around 100 ml of altered blood was evacuated slowly. Gentle saline irrigation was used to remove any remnant clots and blood products. Hemostasis was achieved and the wound closed without a drain.
Figure 1: Computed tomography (CT) scan showing left fronto-temporo-parietal chronic subdural hematoma (CSDH) with a moderate midline shift

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His neurological examination in the immediate postoperative period revealed bilateral ptosis with normal extraocular movements, and bilaterally equal and reactive pupils [Figure 3]. The patient's sensorium and right limb weakness also improved. Based on the clinical findings we inferred the lesion to be at the site of the unpaired midline nucleus of the third nerve that supplies the levators. This was further confirmed by a CT which revealed a 1 × 1.2 cm sized hematoma in the periaqueductal region of the midbrain [Figure 2]. The patient was treated conservatively and made a gradual recovery. At 6 months follow-up, he shown a remarkable improvement except for the persistence of a mild bilateral ptosis.
Figure 2: Postoperative CT scan showing resolution of the CSDH, and a hematoma in the periaqueductal region of the midbrain (white arrow)

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Figure 3: (a) Clinical photograph showing bilateral ptosis, (b) On elevating the eyelid with a finger, the pupils are normal in size and briskly reactive with no evidence of any extraocular muscle palsy

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An intracerebral hematoma is a rare complication that they may develop following the evacuation of a CSDH. There is very little published data regarding this entity. Kotwica and Brzeziński [1] and Richter et al., [2] have reported an incidence of 0.7-5%. There is no previous report of an intracerebral hematoma developing in the midbrain after evacuation of a CSDH in the published English literature.

The oculomotor nerve arises from the oculomotor nuclear complex in the midbrain and conveys motor fibers to extraocular muscles and levators of the eyelid, and parasympathetic fibers to the pupil. The nucleus is situated in the periaqueductal gray matter just anterior to the aqueduct of Sylvius, at the level of the superior colliculi. Each oculomotor nucleus consists of multiple adjacent subnuclei that innervate specific ocular muscles. The paired lateral nuclei are the largest and are situated anterior and lateral to others; their medial portions are fused into an unpaired mass. A single midline structure, the central caudal nucleus, supplies the levator palpebrae muscles on both sides. The periaqueductal gray matter is also involved influencing the eyelid function; its destructive lesions may cause ptosis. [3]

The symptoms of an intracerebral hematoma may occur either immediately or several days after evacuation of a CSDH. The hematoma can either be adjacent to the location of the CSDH or at a remote site, as occured in our case.

The underlying pathophysiology of this entity has not been clearly elucidated. Evaluation of blood flow changes in patients with a CSDH using positron emission tomography has demonstrated decreased blood flow at remote sites like the thalamus and the basal ganglia that is followed postoperatively by a normalization of blood flow. [4],[5] It has been hypothesized that sudden restoration of normal pressure in regions of faulty cerebral vascular autoregulation due to a subcortical swelling, underlying surface compression, focal impedance of the venous drainage, or ischemic loss of CO 2 reactivity may in turn lead to vascular damage that results in an intraparenchymal hematoma. [6] Damage to the cerebral vasculature secondary to a perioperative parenchymal shift, a sudden increase in the blood flow combined with a defective vascular autoregulation, and hemorrhage into a previously undetected contusion have also been proposed to explain the occurrence of a delayed intracerebral hematoma or a SDH. [7],[ 8] Long-term use of antiplatelet agents may lead to an altered coagulation state and precipitate a remote hemorrhage. [9]

A slow evacuation of the hematoma is, therefore, of paramount importance and can reduce the incidence of this catastrophic complication.

  References Top

Kotwica Z, Brzeziński J. Chronic subdural haematoma treated by burr holes and closed system drainage: Personal experience in 131 patients. Br J Neurosurg 1991;5:461-5.  Back to cited text no. 1
Richter HP, Klein HJ, Schafer M. Chronic subdural haematomas treated by enlarged burr-hole craniotomy and closed system drainage. Retrospective study of 120 patients. Acta Neurochir (Wien) 1984;71:179-88.  Back to cited text no. 2
Campbell WW. DeJong`s The Neurological Examination. 7 th ed. Philedelphia: 19103 USA: Wolters Kluwer (India) Pvt Ltd, New Delhi; 2013.  Back to cited text no. 3
Ishikawa T, Kawamura S, Hadeishi H, Suzuki A, Yasui N, Uemura K. Cerebral blood flow and oxygen metabolism in hemiparetic patients with chronic subdural hematoma: Quantitative evaluation using positron emission tomography. Surg Neurol 1995;43:130-7.  Back to cited text no. 4
Tanaka A, Kimura M, Yoshinaga S, Ohkawa M. Computed tomography and cerebral blood flow correlations of mental changes in chronic subdural hematoma. Neurosurgery 1992;30:370-7.  Back to cited text no. 5
Ulivieri S, Oliveri G. Intracerebral haemorrhage following surgical evacuation of chronic subdural haematoma: Case report. G Chir 2008;29:233-4.  Back to cited text no. 6
Cook AW, Browder EJ, Carter WB. Cerebral swelling and ventricular alterations following evacuation of intracranial extracerebral hematoma. J Neurosurg 1962;19:419-23.  Back to cited text no. 7
Kim SS, Cheong JH, Kim JM. Massive intracerebral hemorrhage following drainage of subdural hygroma. J Korean Neurosurg Soc 2007;41:267-8.  Back to cited text no. 8
Rojas-Medina LM, Goel A. Brainstem hemorrhage secondary to evacuation of chronic sub dural hematoma. Neurol India 2014;62:435-7.  Back to cited text no. 9
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