There were some differences on knowledge, attitudes, and spiritual history skills between students who participated in the S/H teaching strategy and students who have not been exposed to the theme. These results might foster discussion for the development of new educational strategies about the subject.

Case Presentation Female, 62 years old, history previous of hypertension and multiple cavernomatosis, admitted to our service emergency room with hypothesis of stroke. The patient presented headache associated with nausea and phosphenes in the right eye, with evolution for right hemiplegia. However, she showed complete and spontaneous reversal of symptoms, in a few minutes. The patient presented similar symptoms with annual recurrence since 2019, always following migraine attack. She denied familiar history of migraine. Brain MRI showed multiple cavernomatosis, with no signs of old or recent ischemia. Brain and cervical CT angiography and laboratorial tests were normal. She was then diagnosed with sporadic hemiplegic migraine, with no family report of the disease. She received treatment with Amitriptyline 50 mg per day, without further recurrences. Discussion Hemiplegic migraine (HM) is a rare form of migraine with motor aura, which includes fully reversible motor weakness. The aura of HM is most probably caused by cortical spreading depression, a self-propagating wave of neuronal and glial depolarization that spreads across the cerebral cortex. Patients who are the first member of their family to have hemiplegic migraine are classified as having sporadic hemiplegic migraine. Some cases of sporadic hemiplegic migraine are caused by one of the genetic variants that cause familial hemiplegic migraine. The treatment of HM is empirical and mainly relies on principles of management of the common types of migraine, except for triptans use, medication historically contraindicated because of vasoconstrictor properties. Final comments Hemiplegic migraine is an important differential diagnosis with stroke in patients with migraine. Correct recognition of this condition can be a crucial factor in the treatment and prognosis of the patient in the emergency room.   Keywords: hemiplegic migraine, motor aura, stroke mimics.

Case presentation Female, 18 years-old, without relevant family history, referred to Neurology by Hematology for headache. 3 years ago, she was diagnosed with Acute Promyelocytic Leukemia (APL) currently on maintenance therapy with All-Trans Retinoic Acid (ATRA). The patient reports that in all previous cycles presented headache with the following characters: one-side temporal location, pulsating quality, moderate intensity, with nausea and vomiting, photophobia and phonophobia, uncertain duration, with simple analgesics response. In the current cycle, she relates continuous pain, severe intensity and unresponsive to medication. On examination, there were no focal neurological findings and on funduscopic examination there was no papilledema. MRI and laboratorial tests were normal. Cerebrospinal fluid (CSF) opening pressure was 35 cmH2O, no other alterations. 15 milliliters of CSF were removed, with a closing pressure of 25 cmH2O. A hypothesis of Intracranial Hypertension associated with use of ATRA was made. Afterwards, there was important improvement of the headache, with residual pain of mild intensity. Therefore, Acetazolamide was started at a dose of 250 milligrams every 12 hours with complete resolution of symptoms.   Discussion Acute myeloid leukemia (AML) comprises a heterogeneous group of aggressive blood cell cancers that arise from clonal expansion of malignant hematopoietic precursor cells in the bone marrow. Acute promyelocytic leukemia (APL) is a biologically and clinically distinct variant of AML. APL is classified as acute promyelocytic leukemia with PML-RARA. The cytogenetic hallmark of APL is a translocation involving RARA, the retinoic acid receptor alpha locus on chromosome 17. Without treatment, APL is the most malignant form of AML, with a median survival of less than one month. (To see the complete abstract, please, check out the PDF).

Introduction Spontaneous intracranial hypotension (SIH) is a secondary cause of headache often misdiagnosed and underdiagnosed disorder. The main presentation is orthostatic headache. An uncommon symptom is cranial nerve palsy. We described a case of SIH that presented to our service with sixth cranial nerve palsy. Case Report Female, 39 years old, no relevant medical past or history of trauma, awoke due intense holocranial headache, associated with vomiting and photophobia, worsening in orthostasis. In the general emergency department, she was release with prescription of analgesics and topiramate, without resolution. After a week, the patient reported diplopia and was referred to our service, a tertiary center. In admission, she kept an intense orthostatic headache and in neurologic examination she presented right sixth nerve palsy, no other deficits. Laboratorial tests were normal, including metabolic and infectious marks. Cerebrospinal fluid (CSF) opening pressure was low (50 mmH2O) and analysis showed elevated protein levels (158mg/dl). MRI showed diffuse pachymeningeal enhancement and venous sinus distension, mainly in superior sagittal venous sinus. CT myelogram detected a spinal CSF leak in transition C1-C2. Initially, performed hydration and bed rest, while patient with partial improvement of headache. An epidural blood patch was then performed using 15ml of autologous blood with compatible contrast and lidocaine. There was complete resolution of pain after the procedure and four weeks later complete resolution of right sixth nerve palsy. Discussion According to International Classification of Headaches Disorders, third edition (ICHD-3), the headache attributed to SIH is descripted as a headache has developed in temporal relation to low CSF pressure (<60mm H2O) and/or evidence of CSF leakage on imaging.   (To see the complete abstract, please, check out the PDF).

Cases reports: Two females from different families, 34 and 16 years old, who started at puberty with distal weakness in lower limbs and difficulty in walking. The youngest had a history of parental consanguinity. The oldest also developed symptoms of cerebellar ataxia. Both patients had joint hypermobility. After physical exercise, both showed increased serum levels of creatine phosphokinase, but only one of them showed increased lactate. Both electroneuromyography showed motor neuropathy, predominantly in lower limbs, with axonal and demyelinating pathophysiology, with probable superimposed pre-ganglionic involvement. Both genetic tests showed homozygous pathogenic variation in COQ7 gene, described as Chr16:19.067.667, which leads to methionine substitution and impaired protein traduction. Discussion: Primary COQ10 deficiency is a heterogeneous group of mitochondrial disorders caused by defects in proteins involved in COQ10 biosynthesis. It’s inheritance usually is autosomal recessive. Mutations in 10 genes directly involved in coenzyme Q10 synthesis and collectively named “COQ genes” have been identified. Clinical spectrum may overlap encephalomyopathies, ataxia, neuromyopathy, spastic paraplegia and even impairment of another organs. Only four COQ7 deficiency patients have been reported so far. In addition, cases reported here are related with a new variation in COQ7 gene. All reported COQ7 deficiency patients have asian ancestry, which is not the case of patients related here. Some improvement can occur by COQ10 supplementation, which was initiated in both cases. Conclusion: The diagnosis of primary COQ10 deficiency is limited by factors like rarity, heterogeneous phenotypes and unavailability of genetic testes, which favors under or misdiagnosis. Discovery of new cases and mutations can increase our knowledge about this condition, make possible the diagnosis, consequently look for dysfunction of other organs and try a specific treatment.