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In the last decades, many neuroimaging studies have investigated the brain structural deficits associated with the pathophysiology of Bipolar Disorder (BD). Notably, the available literature identified the presence of selective brain structural abnormalities, in terms of both gray matter (GM) and white matter, known to be involved in emotion regulation and processing. Nonetheless, the complex and heterogeneous nature of BD has not yet allowed the identification of a clear biological signature of this disorder. In this context, this review aims to a) briefly summarize the evidence from structural Magnetic Resonance Imaging (MRI) studies on BD in order to provide a clearer picture of the neural circuits involved in this disabling mental illness, and b) describe some critical clinical issues that need to be taken into account when studying BD, especially the history of psychosis and the link between BD and behavioral variant fronto-temporal dementia (bvFTD). Evidence from structural MRI studies on BD suggests ventricular, prefrontal and temporal abnormalities but remain largely inconsistent, possibly reflecting the disorder complexity. Moreover, the reviewed evidence showed that psychotic BD might represent a subtype of the disorder with specific and enhanced alterations of GM morphology. Finally, from the available MRI evidence exploring the relationship between BD and bvFTD emerged the need of a differential identification of biological markers to enable the early and accurate detection of the two disorders, ultimately guaranteeing a better prognosis and the employment of more targeted and effective treatments.

Balò's concentric sclerosis (BCS) is considered a rare demyelinating disease and regarded as an aggressive variant of multiple sclerosis (MS). We describe three cases (one male and two females) with neuroimaging features suggestive of BCS and heterogeneous symptoms, with benign long-term clinical course upon treatment with natalizumab and fingolimod. Neurological examination, blood and cerebrospinal fluid analyses, brain and spinal cord magnetic resonance imaging (MRI) and brain proton magnetic resonance spectroscopy were performed. At onset, patient #1 showed predominant cognitive impairment with consciousness disturbances; patient #2 presented with left hemiparesis; patient #3 demonstrated hesitance in speech and in written word production, along with right central facial palsy. All patients showed the typical MRI changes associated with BCS, such as concentric rings or a whorled appearance on T2-weighted and contrast-enhanced T1-weighted images. They were treated with high dosage i.v. steroid with clinical improvement and followed-up for 3 years with different clinical course. Two patients fulfilled the revised McDonald criteria for MS and received preventive therapy, natalizumab and fingolimod, respectively, whereas the third patient is still stable without clinical and radiological evolution. All of them did not have new exacerbations or MRI lesions over 2-4 year follow-up. Our descriptions demonstrate the heterogeneity of clinical presentation of BCS. Moreover, these case reports suggest that BCS may neither be rapidly progressive nor fatal and may be considered part of the MS spectrum. In line with this hypothesis, current treatments for MS were effective in our patients.

Many causes of traumatic sciatic neuropathy have been described in the literature [1], but extrapelvic endometriosis of the gluteal region presenting as sciatica remains difficult to recognize. Here, we present the case of a 45-year-old woman with a history of lower back pain and lower limb stiffness in whom hip MRI showed multiple loci of endometriosis localized in both iliac muscles and in the right gluteus. The woman presented with a 15-day history of lower back pain and impaired ambulation. Neurological examination showed lower limb stiffness with left leg flexure and right leg hyperextension, right foot dorsiflexion deficit, positive Lasegue sign, gait disturbance and severe pain with apparent (L4)-L5-S1 distribution. An EMG and a spinal cord MRI scan had previously been performed without any pathological findings. Intravenously administered myorelaxants and NSAIDs were tried without any benefit. Her past medical history was consistent only with diabetes. Routine blood tests showed only mild anaemia and high cancer antigen-125 (CA-125) levels. Brain and spinal cord MRI, backbone CT, and total-body PET scans did not show any pathological findings. Orthopaedic examination showed groin pain, irradiating to the knee and worsened by hip movement. On MRI T2-weighted images both the iliac and psoas muscles and the gluteus maximus and minimus appeared markedly bright. In the iliac muscles two T2-hyperintense formations, without contrast enhancement but with a hypervascular rim, were evident; the right gluteus showed similar findings (Fig. 1a). On the 4th day of hospitalization her period started and the patient reported worsening pain and severe abdominal cramps. Gynaecological examination showed a 2-cm fibrotic nodule in the pouch of Douglas, suggestive of endometriosis. CA-125 was 49.3 IU/ml (cutoff 35 IU/ml). A cycle of leuprorelin (a gonadotropinreleasing hormone agonist which downregulates the secretion of gonadotropin luteinizing hormone and folliclestimulating hormone leading to hypogonadism) was started, and thereafter symptoms slowly resolved. A follow-up MRI scan performed 3 months later showed a reduction in size and number of the lesions; neurological examination was normal (Fig. 1b). In accordance with previous report [1], CA-125 was elevated in our patient. The marked T2 brightness in both the iliac and gluteus muscles seen on the MRI scan was consistent with oedema and hyperaemia or, as described previously [2], neurogenic muscular injury. This finding may be suggestive of an endometriosic lesion localized at or near the sciatic notch. The T2-hypentense formations were consistent with foci of endometriosis localized in the muscle tissues. The cyclicity of the symptoms and their regression after a cycle of leuprorelin further supports our hypothesis [3, 4]. Endometriosis-induced cyclic sciatica was firstly reported by Schlincke in 1946 [5]. Since then, approximately 60 cases have been described. Lesions of the ipsilateral sciatic nerve are reported as the primary cause of almost all the endometriosis-induced cyclic sciatica [6]. The commonest localization is the sciatic notch where fibrosis, organized haematoma and endometrial tissue L. Ghezzi (&) A. Arighi A. M. Pietroboni F. Jacini G. G. Fumagalli N. Bresolin D. Galimberti E. Scarpini Department of Neurological Sciences, ‘‘Dino Ferrari’’ Center, Fondazione Ca Granda, IRCCS Ospedale Maggiore Policlinico, University of Milan, Milan, Italy e-mail: lauraghezzi@me.com