2017年 · 第50卷第03期

amyloid spells, also known as transient focal neurological events (TFNE), were first started by Greenberg et al. in 1993^[1]It is reported that as one of the main clinical manifestations of patients with cerebral amyloid angiopathy (CAA) without lobar cerebral hemorrhage, it is related to focal cortical hemorrhage (petechial hemorrhage), which has been gradually recognized as another important clinical feature of CAA in recent years. CAA is a kind of age-related disease in which chronic progressive β-amyloid (A β) is deposited in cerebral cortex and small vessels of leptomeningeal. It is currently recognized as the most common cause of non-traumatic recurrent lobar hemorrhage^[2]It is also one of the important reasons for cognitive decline in the elderly^[3]。 At present, the Boston diagnostic criteria of CAA have been used clinically. The diagnostic criteria divide CAA into four types according to clinical, imaging and pathological features: definite CAA, probable CAA with supporting pathology, probable CAA and possible CAA. The sensitivity and specificity of this diagnostic criterion have been verified, and it has been widely used in clinical and research^[4]。 The revised diagnostic criteria in 2010 included cortical superficial siderosis (cSS) as an important marker in imaging diagnosis together with symptomatic lobar hemorrhage^[5]。 In fact, although CAA is not uncommon, the clinical awareness rate is not optimistic, Charidimou et al.^[6]In a review in 2013, it was mentioned that:Journal of Neurology Neurosurgery&PsychiatryThe results of a questionnaire survey of doctors in the magazine showed that about 80% of stroke doctors were under-recognized. With the progress of imaging, the understanding of CAA is gradually deepening. More and more clinical observations have found that in addition to recurrent lobar hemorrhage and chronic progressive cognitive decline, CAA patients can also show TFNE similar to transient ischemic attack (TIA). Recently, some scholars have named it as cerebral amyloid attack^[7]。 Because of its clinical features and its correlation with CAA and the risk of cerebral hemorrhage, this clinical symptom began to gradually attract attention and attract attention.

cerebrovascular disease refers to transient or permanent cerebral dysfunction caused by lesions in one or more cerebral blood vessels due to various causes^[1]。 stroke (stroke) is an acute cerebrovascular disease, which is an acute focal vascular neurological deficit syndrome. The symptoms last for more than 24 hours or die, and other non-vascular causes are excluded^[2,3]。 The classification and classification of cerebrovascular diseases has important practical value for accurate clinical diagnosis of diseases and accurate selection of treatment and preventive measures. It is the basis of diagnosis, differential diagnosis and individualized treatment of cerebrovascular diseases, and it is also the basic need of epidemiological research and clinical research of cerebrovascular diseases. The standardization and unification of classification and classification is beneficial to the comparison of results and academic exchange between studies, and is of great significance to clinical diagnosis and treatment. For a long time, there are many classification methods at home and abroad, but there is no unified standard for clinical practice^[1,2,3,4]In particular, there is a lack of classification standards suitable for China's clinical practice and good operability. Therefore, the Neurology Branch of the Chinese Medical Association in China began to formulate and publish the classification of cerebrovascular diseases about 40 years ago (1978), and so far there are four versions (Table 1)^[5,6,7,8]。 Chinese Cerebrovascular Disease Classification 2015 published in this issue^[8]Through the efforts of two members of the Neurology Branch of Chinese Medical Association and its Cerebrovascular Disease Group, a consensus was reached through many discussions. This edition of the classification is formulated in combination with international standards and China's national conditions as much as possible, taking into account previous use experience and operability. It does not include the corresponding diagnostic points or definitions yet, but a consensus will be formulated and published in the near future. In order to better understand and use the 2015 version of the Chinese classification of cerebrovascular diseases, we interpret the relevant progress as follows.

Excludes: Traumatic intracranial hemorrhage.

Ischemic stroke is one of the most important causes of death and disability in China at present. Among them, acute occlusion of intracranial and extracranial large vessels is a subtype of ischemic stroke with severe disease and poor prognosis, resulting in huge social and economic burden^[1]。 Intravenous application of recombinant human tissue type plasminogen activator (rt-PA) within 4.5 h has been widely used worldwide as the most well-documented treatment for acute ischemic stroke^[2,3]； However, due to its relatively strict time window and indication and contraindication requirements, the proportion of patients receiving thrombolytic therapy is relatively low^[4]。 In addition, a considerable proportion of large vessel occlusive strokes are not sensitive to rt-PA, and only 6% ~30% can achieve occlusive vessel recanalization, with limited benefit^[5]。

cervical artery dissection (CAD) is a common cause of stroke in young people. Delay in diagnosis or treatment can lead to acute ischemic stroke, focal neurological deficit, and even coma. Clinically, it is rare for patients to develop bilateral carotid artery dissection simultaneously. We report the treatment and follow-up of a patient with bilateral internal carotid artery dissection (internal carotid artery dissection) with ischemic stroke, and analyze it with literature review.

Toxoplasma gondii encephalopathy is an opportunistic infectious disease caused by Toxoplasma gondii parasitizing the brain. It is also one of the most common complications in patients with immunodeficiency such as acquired immunodeficiency syndrome, organ transplantation and long-term immunosuppressant use^[1]。 Toxoplasma gondii encephalopathy complicated with extracranial malignant tumor is rare^[2,3]And is easily misdiagnosed as intracranial metastases. A case of toxoplasma encephalopathy complicated with lung adenocarcinoma and liver and spleen metastases admitted to our hospital is reported as follows.

crossed cerebellar diaschisis (CCD) refers to a decrease in blood flow, a decrease in glucose oxidative metabolism, or even crossed cerebellar atrophy (CCA) in the contralateral cerebellar hemisphere when one cerebral hemisphere is diseased. CCD was initially reported in patients with cerebral infarction. Subsequent studies have found that supratentorial tumors, epilepsy, encephalitis and other diseases can cause CCD^[1]。 We report a patient with CCD caused by status epilepticus detected by MRI of the head, which is summarized below.

posterior cortical atrophy (PCA), also known as Benson syndrome, was first reported by Frank Benson in 1988. It is a rare progressive neurodegenerative disease with advanced visual impairment as the first symptom. Finally, patients will develop visual spatial and visual perception impairment, anexia, Balint syndrome and Gerstmann syndrome as the main clinical manifestations. Memory and language fluency were not significantly affected in the early stage of the disease, and the typical onset age was 50-65 years old. The main imaging features were posterior cortical atrophy and posterior cortical metabolism decrease^[1,2,3]。 Although PCA has been recognized for more than 20 years, it is still often misdiagnosed or missed. Domestic clinical and imaging of PCA, especially¹⁸F-fluorodeoxyglucose (FDG) PET and¹¹Few reports on the characteristics of C-Pittsburgh complex (PIB) PET imaging. One patient with PCA admitted to us is reported as follows, and the clinical and imaging features of PCA are summarized.

transient focal neurologic events are a general term for clinical episodic symptoms, including transient ischemic attack, aura migraine, partial seizure, subdural hematoma, demyelinating disease, intracranial tumor, central nervous system infection, hypoglycemia, etc. The common characteristics of these events are that the clinical symptoms are transient and recurrent, but the clinical manifestations are wide, including sensory, motor, speech, visual symptoms, etc. The pathological mechanism and treatment methods are also very different. The characteristic manifestations and treatment schemes of different attack types need standardized diagnosis and in-depth research urgently^[1]。

cerebral microbleeds in magnetic resonance gradient echo T₂⁺Weighted sequence (gradient-echo T₂⁺-weighted imaging) and susceptibility weighted imaging (susceptibility weighted imaging), showing homogeneous circular or oval signal loss with a diameter of 2 to 5 mm (<10 mm), No peripheral edema^[1]。 It is usually related to the etiology of hypertensive arteriolopathy or cerebral amyloid angiopathy (CAA). The former causes microhemorrhage in the deep part of the brain including basal ganglia, thalamus, cerebellum, brainstem and other parts, while the latter is mostly localized in the lobes^[2,3,4]。 Previously, the incidence of cerebral microhemorrhage has been reported to be 3% to 7% in healthy people, 35% to 71% in ischemic stroke, and up to 50% to 80% in hemorrhagic stroke, and is associated with the risk of bleeding and the recurrence of ischemic stroke^[5,6,7,8]。

amyotrophic lateral sclerosis (ALS) is a fatal neurodegenerative disease of unknown etiology that mainly involves motor neurons in the cerebral cortex, brainstem, and spinal cord^[1]The clinical manifestations are local muscle weakness, atrophy, and pyramidal tract signs with invasive onset and progressive progression to paralysis of all skeletal muscles. Typical patients with ALS mostly die of respiratory muscle paralysis within 3 to 5 years after the onset of the disease. So far, no treatment can change the outcome of the disease. The traditional view believes that ALS is a degenerative disease that specifically damages motor neurons and does not involve sensory nerve system. However, with the continuous enrichment of related research, the view that ALS is accompanied by sensory nerve damage is increasing day by day. We reviewed the research progress of sensory nerve damage in ALS in recent years.

Parkinson's disease (Parkinson's disease) is a common neurodegenerative disease, with bradykinesia, tremor, rigidity and abnormal gait posture as the main clinical manifestations. The prevalence rate of the elderly over 65 years old in China is about 1.7%^[1]。 The classical pathophysiological theory of Parkinson's disease holds that the loss of dopamine neurons in substantia nigra and abnormal striatal function may lead to bradykinesia in Parkinson's disease, but it is difficult to explain the neural basis of abnormal gait posture. Studies suggest that gait abnormality in Parkinson's disease may not be a single clinical phenomenon, but a clinical syndrome caused by different underlying mechanisms^[2]。 We present a review of gait abnormalities in Parkinson's disease, focusing on gait abnormalities that are ineffective in treatment and their brain network and neural circuit mechanisms.