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REVIEW ARTICLE
Year : 2022 | Volume
: 8
| Issue : 4 | Page : 188-191
Spontaneous chronic subdural hematoma as the cause of oculomotor cranial nerve palsy: A narrative review
Francesco Pellegrini1, Emanuela Interlandi2, Alessandra Cuna3, Daniela Monaco4, Andrew G Lee5
1 Department of Ophthalmology, “Santa Maria degli Angeli” Hospital, ASFO, Pordenone (PN), Italy
2 Department of Ophthalmology, Ospedale del Mare, ASL Napoli 1 Centro, Naples, Italy
3 Department of Ophthalmology, “De Gironcoli” Hospital, AULSS2 Marca Trevigiana, Conegliano (TV), Italy
4 Emergency Neurology and Stroke Unit, Santo Spirito Hospital, ASL Pescara, Pescara, Italy
5 Department of Ophthalmology, Blanton Eye Institute, Houston Methodist Hospital, Houston; Department of Ophthalmology, University of Texas Medical Branch, Galveston; University of Texas MD Anderson Cancer Center, Houston; Texas A and M College of Medicine, Bryan, TX; Department of Ophthalmology, Neurology, and Neurosurgery, Weill Cornell Medicine, New York, NY; Department of Ophthalmology, The University of Iowa Hospitals and Clinics, Iowa City, Iowa, USA
Correspondence Address:
Francesco Pellegrini
Department of Ophthalmology, "Santa Maria degli Angeli" Hospital, ASFO, Pordenone (PN)
Italy
Source of Support: None, Conflict of Interest: None
CheckDOI: 10.4103/bc.bc_42_22
Acute complete third nerve palsy with pupillary involvement is usually caused by a posterior communicating artery aneurysm (i.e. “the rule of the pupil”). The pupillary fibers run peripherally in the third nerve and are thus susceptible to the external compression. Headache is usually present, and urgent diagnosis and treatment are warranted. Rarely, however, neuroimaging shows other causes of third nerve palsy. In this study, we perform a literature review of spontaneous chronic subdural hematoma that, although rarely, may cause an acute pupil-involving third nerve palsy as a false localizing sign. We review the localizing, nonlocalizing, and false localizing nature of ocular motor cranial nerve palsy in this setting.
Keywords: Acute subdural hematoma, chronic subdural hematoma, Kernoan phenomenon, third nerve palsy
Subdural hematoma (SDH) is a collection of blood under the duramater and is usually classified as acute SDH (ASDH) or chronic SDH (CSDH). ASDH is often traumatic and is often more difficult to treat. ASDH is more likely to produce significant short-term and long-term consequences or death (more than 50% of cases). In contrast, CSDH often presents more insidiously with progressive worsening of consciousness. Neuro-ophthalmic manifestations of CSDH include cranial nerve dysfunction, papilledema from increased intracranial pressure (ICP), and visual acuity loss associated with visual field defect. Among the cranial nerves possibly involved, either third, fourth, or sixth nerve palsy may occur. Although third nerve palsy (TNP) in adults is often caused by ischemia, aneurysm, trauma, and neoplasms. We review the literature on TNP in CSDH and define the localizing, nonlocalizing, and false localizing presentations.
Pellegrini et al. reported a 67-year-old male presented to the emergency room with acute onset headache, ptosis of the left eyelid, and binocular diplopia. Examination showed a left third nerve palsy [Figure 1], and contrast computed tomography (CT) and CT-angiography of the brain revealed a left SDH with a midline shift to the right [Figure 2]. He was urgently treated with craniotomy without sequelae in the neurosurgery department and recovered in 1 month. Patients with SDH may have increased ICP that could produce a nonlocalizing TNP.[1]
Figure 1: Examination revealed left ptosis, large angle exotropia in primary position. Examination of extrinsic ocular movements showed reduced adduction, elevation and depression OS. Reproduced with permission from[1]
Figure 2: Urgent CT of the brain revealed a left CSDH (arrows) with right midline shift to the right (dotted arrows). Reproduced with permission from.[1] CSDH: Chronic subdural hematoma, CT: Computed tomography Methods A literature search was carried out looking for all relevant articles published in the English language Literature since January 1970. The database searched was PubMed. The keywords used were “Third nerve palsy,” “Subdural hematoma,” “Kernohan notch phenomenon” and “Chronic Subdural Hematoma.” Data extracted from each case included age, gender, visual acuity, surgical or medical therapy, and outcome [Table 1].
Table 1: Summary of the literature: Third nerve palsy in subdural hematoma Discussion SDH is defined as a blood collection between the duramater and the arachnoid.[2] ASDH occurs <72 h old with a typically hyperdense aspect on a noncontrast cranial CT scan. CSDH occurs gradually and is characterized by a CT hypodense lesion compared with the normal brain.[3] It is common among elderly patients, especially those who take antiplatelet and anticoagulant drugs after coronary heart disease and cerebral infarction, normally occurring after a mild head injury.[4]
The most frequent clinical manifestations of the CSDH include headache, gait and consciousness disturbances, personality changes, urinary incontinence, and dementia.[5],[6] Neuro-ophthalmic manifestations of CSDH include loss of visual acuity and/or visual field defect, papilledema due to an increased ICP, and cranial nerves, third or sixth dysfunction.[7] To our knowledge, only 15 prior cases of TNP associated with CSDH have been described, as summarized in [Table 1]. Pupil involvement was frequently reported (87.5%), while pupil-sparing was described in two cases (12.5%) of TNP.[8]
Most causes of TNP in adults (e.g. ischemia, aneurysm, trauma, inflammation, neoplasm, and diabetes mellitus).[9] Among symptomatic patients, 62.5% (n = 10 out of 16) manifested at least one other neurological sign, such as decreased level of consciousness in 31% of them (n = 5 out of 16), hemiparesis, ataxia, and visual loss while an isolated TNP represented the only neurologic sign in 37.5% of cases (n = 6 out of 16), with a third nerve involvement ipsilateral to the CSDH. Our case presented with a neurologically isolated TNP, keeping a preserved level of consciousness and good cognitive performance. Thus, a normal level of consciousness does not rule out CSDH. In all reported cases, the rate of recovery after neurosurgery for CSDH was complete in 68.75%, partial in 25%, and absent in 6.25% of cases. An interesting aspect to highlight in reconsidering the clinical manifestations of these patients is linked to the “Kernohan notch phenomenon,” the knowledge of whom is mandatory to better interpret the clinical manifestation and its related cerebral focal involvement. Kernohan and Woltman described this phenomenon in 1929 as a false localizing neurological sign determined when a supratentorial space-occupying lesion, causing mass effect and midline shift, compresses the contralateral corticospinal tract in the cerebral peduncle against the tentorium notch.[1],[10] As the third cranial nerve can be compressed at the level of the tentorium, an ipsilateral motor deficit is provoked, while classically, in uncal herniation, an ipsilateral pupil dilation with contralateral hemiparesis is documented (i.e. the Kernohan notch phenomenon).[11] Thus, a TNP could be led to an erroneous interpretation in a CSDH condition, false lateralizing (i.e. the lesion can be contralateral) and false localizing (i.e. an infratentorial lesion along the course of the third nerve) of the side of the lesion.[22]
ConclusionsClinicians should be aware that TNP can be a localizing, nonlocalizing, or false localizing finding in ASDH and CSDH. The most feared localizing cause of a painful, pupil-involved TNP is the ipsilateral posterior communicating aneurism (PCOmA). TNP caused by CSHD is relatively rare and can occur with or without loss of consciousness, hemiparesis, or other cranial nerve involvement. The TNP, however, may be nonlocalizing due to increased ICP or false localizing in the case of herniation and the Kernohan notch phenomenon.
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