Data on bilateral chronic subdural hematomas (CSHs) are scant 1) , including information on the frequency of symptoms, response to various treatments, and postoperative complications, compared with data on unilateral CSH. Bilateral CSHs constitute a fair portion of CSHs, especially in patients older than 75 years and in those with coagulopathy.
The frequency of focal neurological deficits was found to be lesser in patients with bilateral CSDH, and it may confound the diagnosis and delay treatment 2).
Bilateral hematomas may lead to medial compression of both ventricles resulting in a narrow, slit-like elongated ventricle (the anterior horns sharply pointed and approaching one another so called ‘squeezed ventricle,’ ‘hare’s ears sign, or ‘rabbit’s ears’) 3) 4)5) 6).
see also Bilateral isodense chronic subdural hematoma
Magnetic resonance imaging
Treatment of bilateral CSHs presents its own unique set of problems. New hemorrhage on the contralateral side and shift of midline structures are concerns and can be avoided by simultaneous bilateral decompression 12) 13). and significantly lowers the risk of retreatment compared with unilateral intervention and should be considered when choosing a surgical procedure 14).
To prevent neurological deterioration resulting from the thicker hematomas, early surgical decompression for bilateral CSDH should be implemented 15).
Clinicians must be aware of the higher recurrent rate of bilateral CSDH after burr hole craniostomy 17).
In bCSDHs bilateral surgical intervention significantly lowers the risk of retreatment compared with unilateral intervention and should be considered when choosing a surgical procedure 18).
Ninety-three patients with bilateral CSDH who underwent unilateral bur hole surgery at Aizu Chuo Hospital were included in a retrospective analysis. Findings on preoperative MRI, preoperative thickness of the drained hematoma, and the influence of antiplatelet or anticoagulant drugs were considered and evaluated in univariate and multivariate analyses.
The overall growth rate was 19% (18 of 93 hematomas), and a significantly greater percentage of the hematomas that were iso- or hypointense on preoperative T1-weighted imaging showed growth compared with other hematomas (35.4% vs 2.3%, p < 0.001). Multivariate logistic regression analysis showed that findings on preoperative T1-weighted MRI were the sole significant predictor of hematoma growth, and other factors such as antiplatelet or anticoagulant drug use, patient age, patient sex, thickness of the treated hematoma, and T2-weighted MRI findings were not significantly related to hematoma growth. The adjusted odds ratio for hematoma growth in the T1 isointense/hypointense group relative to the T1 hyperintense group was 25.12 (95% CI 3.89-51.58, p < 0.01).
The findings of preoperative MRI, namely T1-weighted sequences, may be useful in predicting the growth of hematomas that did not undergo bur hole surgery in patients with bilateral CSDH 19).
The mean Markwalder grading score at admission was 1.89 ± 0.66 and 1.64 ± 0.49 in the unilateral and bilateral hematoma groups, respectively (p = 0.010). After a minimum follow-up period of 6 months, the mean Glasgow Outcome Scale was not significantly different (p = 0.060). The recurrence rate of up to 28.00% observed for the bilateral disease was found to be higher than 9.59% observed for the unilateral disease (p = 0.042) 20).
This case report illustrates that the stability of the intracranial pressure should be closely monitored during the surgical treatment of chronic subdural hematomas, and large fluctuations in the cerebral perfusion pressure should be avoided during the operation. They also propose improvements in the technical details of the operative treatment of chronic subdural hematomas 21).
Calcified chronic subdural hematomas are an occurrence rarely seen in neurosurgical clinical practice. And when they occur bilaterally, the radiologic image they present is fascinating, as is the clinical presentation, but their management may be challenging. They have been reported to present with a multitude of neurologic deficits but never with diabetes insipidus, which is described by Siddiqui et al.
Due to the rarity of this pathology, the management protocol is not well defined, though there have been quite a few papers on this condition. This review article gathers information published over the years on this rare entity to suggest a treatment protocol 22).
Two months later he developed progressive deterioration in mobility. His wife noted an increasing level of forgetfulness and intermittent episodes of confusion. His general practitioner noted a shuffling gait and rigidity affecting lower limbs and made a working diagnosis of parkinsonism. A trial of Madopar (Levodopa and benserazide: 62.5 mg three times a day for 2 weeks) was given by the GP but this failed to improve the situation and he became virtually bed-bound. He was referred back to the hospital for further investigation.
On admission he was confused and marked rigidity affecting upper and lower limbs was detected. No resting tremor was noted but gait could not be tested, as he was unable to get out of bed. In view of the clinical presentation a computerized tomography scan of the head was repeated which showed bilateral fronto-parietal chronic subdural haematoma (Figure 1a,b). He was referred to the regional neurosurgical centre where he underwent bilateral burrhole drainage. Postoperative recovery was unremarkable and on examination there was complete resolution of previous rigidity affecting upper and lower limbs. He was able to converse normally with his wife and began walking with the aid of a stick by third postoperative day. A week later he was discharged from the hospital having regained his previous level of mobility and independence with activities of daily living 23).