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Several diseases produce symptoms similar to those of a cerebral stroke, resulting in their misdiagnosis as stroke. Cerebral stroke mimics are common in emergency rooms. We report two cases of cerebral stroke mimics to attract the attention of clinicians, especially emergency room doctors. In one case, a patient with spontaneous spinal epidural hematoma (SSEH) exhibited lower-right limb numbness and weakness. In the other, a patient with spinal cord infarction (SCI) had numbness and weakness of the lower-left limb. Both cases were misdiagnosed as cerebral strokes in the emergency room. One of the patients underwent hematoma removal surgery, and the other received medical treatment for spinal cord infarction. Patients’ symptoms improved, but the sequelae remained. Single-limb numbness and weakness are an uncommon initial presentation of spinal vascular disease that can lead to its misdiagnosis. When encountering single-limb numbness and weakness, it is necessary to consider the differential diagnosis of spinal vascular disease, thereby reducing misdiagnosis.

Rationale: Neurocysticercosis (NCC) can cause lesions across the central nervous system, leading to varying clinical manifestations. While the presentation of nonspecific symptom is rare, they are easy to ignore. The present report documents a case of NCC that manifested as persistent dizziness. Patient concerns: A Chinese woman visited the hospital on account of dizziness, the severity of which had increased gradually over the month prior. Diagnoses: Head computed tomography and magnetic resonance imaging (MRI) revealed hydrocephalus. Cervical MRI revealed an abnormal object in the spinal canal at the junction of the medulla oblongata and C1, which blocked the circulation cerebrospinal fluid circulation and caused the enlargement of the ventricles. Intervention: The patient underwent surgical treatment. The abnormal object was removed, and a diagnosis of NCC was considered by pathological examination. Outcome: The patient's dizziness resolved after surgical treatment, and no other symptoms appeared thereafter. Lesson: Clinicians should not ignore nonspecific clinical symptoms, as they may indicate hydrocephalus.

Rationale: Multifocal cerebral hemorrhage refers to the cerebral hemorrhage in 2 or more lesions at the same time or 48 h in the brain caused by various causes, which has an acute onset, high mortality rate, and poor clinical treatment effect. Subarachnoid hemorrhage (SAH) is caused by the direct flow of blood into the subarachnoid cavity due to the rupture of the diseased vessels at the base or surface of the brain. Cerebral venous sinus thrombosis (CVST) affects approximately 5 people per million and accounts for approximately 1% of all stroke events. CVST with both SAH and multifocal intracerebral hemorrhage (ICH) as the first presentation is extremely rare. Patient concerns: A 57-year-old woman presented with dizziness, nausea, and vomiting. Diagnosis: Neuroimaging confirmed a diagnosis of CVST. Interventions: The patient was treated with dehydration, scavenging free radicals, and nerve protection therapy. Outcomes: After 4 weeks of systematic treatment, the patient resumed independent daily activities and was discharged with only slight non-fluent aphasia. She did not exhibit recurrent thrombosis at an 18-month follow-up point. Main Lessons: The usual treatment for sinus thrombosis is anticoagulation or local thrombolysis. Systemic anticoagulation is the first-line treatment for CVST, even in patients with cerebral hemorrhage or SAH. The present patient's hemorrhage clearly contraindicated heparin; therefore, no anticoagulants or thrombolytic agents were administered during the 4-week hospitalization. We discuss issues for consideration in similar cases and provide an example of determining an individualized approach to treatment.

Rationale: Mild-to-moderate alcoholic cirrhosis of the liver is related to spontaneous intracerebral hemorrhage (ICH). In terms of spontaneous brainstem hemorrhage, pontine is considered as the most common site in contrast to medulla oblongata where the hemorrhage is rarely seen. This rare primary medullary hemorrhage has been attributed so far to vascular malformation (VM), anticoagulants, hypertension, hemorrhagic transformation, and other undetermined factors. Patient concerns: Herein, we describe a 53-year-old patient with 35-year history of alcohol abuse was admitted for acute-onset isolated hemianesthesia on the right side. He was normotensive on admission. A neurological examination revealed isolated hemihypoaesthesia on the right side. He had no history of hypertension, and viral hepatitis, and nil use of anticoagulants. Diagnoses: Brain computed tomography (CT) image demonstrated hemorrhagic lesion in dorsal and medial medulla oblongata which was ruptured into the fourth ventricle. Brain magnetic resonance imaging (MRI), and magnetic resonance angiography (MRA) demonstrated no evidence of VM. The laboratory tests implied liver dysfunction, thrombocytopenia, and coagulation disorders. Abdominal ultrasound, and CT image showed a small, and nodular liver with splenomegaly, suggestive of moderate alcoholic cirrhosis. Interventions: Liver protection therapy and the management of coagulation disorders. Outcomes: After 14 days, he was discharged with mild hemianesthesia but with more improved parameters in laboratory tests. At the 6-month follow-up, brain MRI, MRA, and non-contrast MRI showed no significant findings except for a malacic lesion. Lessons: We conclude that the patient had alcoholic cirrhosis with coagulopathy, and this may have resulted in primary medullary hemorrhage. This is a first case to report alcoholic cirrhosis as etiology of primary medullary hemorrhage.

Rationale: Intracranial vascular atherosclerotic occlusion is one of the most common causes of ischemic stroke world wide. The involvement of large intracranial vessels, in particular, the middle cerebral artery, is usually associated with unfavorable outcomes in patients. Spontaneous recanalization of atherosclerotic occlusion is relatively rare. Patient concerns: The first patient was a 43-year-old male with slurred speech and left-sided weakness for a duration of 24 hours. The second was a 59-year-old male with left-sided weakness over a period of 13 hours. The last was a 49-year-old female patient presented with a 1-month history of right-sided headache. Diagnoses: Atherosclerotic middle cerebral artery occlusion. Interventions: In all cases, oral aspirin (100 mg; once daily), Plavix (75 mg; once daily), and Lipitor (40 mg; once daily) were used . Oral Plavix was stopped 3 months. Outcomes: Spontaneous recanalization occured in the three cases of atherosclerotic middle cerebral artery occlusion. Lessons: Spontaneous recanalization may occur in both early and late stages of atherosclerotic middle cerebral artery occlusion. Clinicians should be aware of this particular condition, as it may represent a relatively favorable prognosis.

PCR amplification and sequencing of whole blood DNA from an individual with hereditary spastic paraplegia, as well as family members, revealed a fragment of proteolipid protein 1 (PLP1) gene exon 1, which excluded the possibility of isomer 1 expression for this family. The fragment sequence of exon 3 and exon 5 was consistent with the proteolipid protein 1 sequence at NCBI. In the proband samples, a PLP1 point mutation in exon 4 was detected at the basic group of position 844, T→C, phenylalanine→leucine. In proband samples from a male cousin, the basic group at position 844 was C, but gene sequencing signals revealed mixed signals of T and C, indicating possible mutation at this locus. Results demonstrated that changes in PLP1 exon 4 amino acids were associated with onset of hereditary spastic paraplegia.