What Is Clinical Neurology?

Neurology is a secondary discipline on neurology. Not a medical concept. Mainly treat cerebrovascular diseases (cerebral infarction, cerebral hemorrhage), migraine, inflammatory diseases of the brain (encephalitis, meningitis), myelitis, epilepsy, dementia, metabolic diseases and genetic predisposed diseases, trigeminal neuralgia, sciatic nerve disease, Peripheral neuropathy and myasthenia gravis.

Neurology

Neurology is about neurology

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  Neurology Facial Paralysis

  Facial nerve palsy (facial neuritis, Bell's palsy, Hunter syndrome), commonly known as "facial palsy", "crooked mouth", "crooked mouth", and "hanging wind" are one of the main features of facial expression muscle group motor dysfunction Common diseases.

  Causes of Neurology

  (1) Infectious lesions (about 42.5%): Most infectious lesions are caused by activation of shingles (VZV) dormant in the dormant state of the facial sensory ganglia;

  (2) Ear-borne diseases;

  (3) Idiopathic (often called Bell's palsy);

  (4) tumor (about 5.5%);

  (5) Neurogenic: about 13.5%;

  (6) Traumatic;

  (7) Poisoning: such as alcoholism. Long-term exposure to toxicants;

  (8) Metabolic disorders: such as diabetes and vitamin deficiency;

  (9) vascular insufficiency;

  (10) Congenital hypoplasia of the facial nucleus;

  Introduction to Neurology Typing

  Facial nerve palsy is divided into central type and peripheral type.

  Central type

  It is caused when the tissues on the nucleus (including the cortex, cortical brainstem fibers, inner capsule, pontine, etc.) are damaged, and the muscles on the contralateral face of the lesion appear to be paralyzed. From the top to the bottom, the nasolabial sulcus becomes shallow, and the mouth angle droops when the teeth are exposed (or the corner of the mouth is skewed to the lesion side, that is, the side of the paralyzed facial muscle). Whistles and drums cannot be blown. More common in cerebrovascular disease, brain tumors and encephalitis.

  Peripheral

  It is caused by the facial nucleus or facial nerve damage, and all facial muscles on the same side of the lesion appear paralyzed. From top to bottom, it can not be frowned, frowning, eyes closed, corneal reflex disappeared, nasolabial sulcus becomes shallow, can not show teeth, bulging gills. Whistling, drooping of the corner of the mouth (or the corner of the mouth is skewed to the opposite side of the lesion, that is, the side of the paralyzed facial muscle). It is more common in peripheral facial paralysis caused by cold, ear or meningeal infection, and neurofibromas. In addition, there may be 2/3 taste disorders before the tongue.

  Clinical manifestations of neurology

  Most patients often find that their cheeks are not working properly and their mouths are skewed when they wash their faces and gargle in the morning. Patients with facial paralysis muscles completely paralyzed, with forehead wrinkles disappearing, eye fissures enlarged, nasolabial sulcus flat, mouth corners drooping, mouth teeth skewed to the healthy side when teeth are exposed. The affected side cannot do wrinkle forehead, frowning, closing eyes, gasping, and pursing. When the gills and whistle are blown, the affected side's lips cannot be closed and the air leaks. When eating, food residues often stay in the tooth-cheek space on the diseased side, and saliva often drips from that side. Due to the inversion of the puncta with the lower eyelid, the tears cannot overflow and drain as normal. It is divided into two types of peripheral and central (see the classification of facial paralysis). The incidence of peripheral facial paralysis is high, and the most common are facial neuritis or Bell's palsy. Facial palsy is usually referred to as facial neuritis in most cases. Facial paralysis can cause very weird faces, so it is often referred to as "disfiguring disease".

  Neurological preventive measures

  1. Eat more fresh vegetables, whole grains, soy products, jujube, lean meat, etc.

  2. Patients with facial paralysis usually need to reduce the stimulation of light sources, such as computers, televisions, and ultraviolet rays.

  3. You need to do more functional exercises, such as raising your eyebrows, inflating your eyes, keeping your eyes closed, and opening your mouth.

  4. Need to insist on acupoint massage every day.

  5. Soak your feet in hot water before going to bed. If possible, do some foot massage.

  6. Appropriate exercise, strengthen physical exercise, often listen to brisk music, feel calm and happy, and ensure adequate sleep.

  7. During the treatment of patients with facial paralysis, avoid spicy food. Such as white wine, garlic, seafood, strong tea, spicy hot pot and so on.

  8. Use a towel to warm your face 3-4 times a night. Do not wash your face with cold water. In cold weather, you need to keep your head warm.

  Neurological treatments

  I. Psychological factors

  Investigations have shown that psychological factors are one of the important factors that trigger facial paralysis. Before the occurrence of facial paralysis, a considerable number of patients had physical fatigue, lack of sleep, nervousness and physical discomfort.

  Second, good mood

  The best way to prevent facial paralysis is to pay attention to maintain a good mood, ensure adequate sleep, and exercise appropriately to enhance the body's immunity.

  Facial palsy is only a symptom or sign. Care must be taken to find the cause. If the cause can be found and treated in a timely manner, such as myasthenia gravis, sarcoidosis, tumors, or temporal bone infections, the process of the primary disease and facial paralysis can be changed. Facial palsy may also be an early symptom of some life-threatening neurological conditions, such as polio or Guillian-Barre syndrome, which can save lives if diagnosed early. The following table shows the signs and possible causes of the different parts of the facial nerve.

  Typical cases of neurology

  Case 1

  Patient male, 60 years old. After being angry, her eyes were suddenly incompletely closed, accompanied by dizziness, poor speech, and no headache or defecation disorder. Examination: no abnormalities in the internal medicine system. Peripheral facial paralysis, active tendon reflexes in the extremities, inaccurate left nose test, and positive Babinski sign were positive. Blood, urine routine, liver function, blood glucose, and erythrocyte sedimentation were normal. ECG showed multiple preatrial contractions and left anterior branch block. CT scan of the head: no abnormalities. Head magnetic resonance (MRI) examination: T1 weighted image showed low signal at the base of bilateral pontine, and T2 weighted image showed high signal, diagnosed as bilateral pontine infarction. After treatment with nerve cell activator, vasodilator, antiplatelet aggregation and other drugs for 1 month, the symptoms and signs improved and he was discharged.

  Case 2

  Patient female, 28 years old. He was admitted for 3 days with crooked mouth, dizziness, headache, diplopia, and numbness in his right limb. Past history, personal history, menstrual history, marriage and childbirth history, and family history were all normal. Experience: BP14 / 8kpa, conscious, normal development, normal medical examination. Nervous system: Eye movement is normal, 0.3cm on the right side of the pupil, 0.4cm on the left side, normal reflection of light, left nasolabial sulcus is slightly shallow, tongue extended slightly to the right, right half body pain, tactile sensation. The right muscle strength was grade IV, tendon reflex (+), right Pap sign (+), and plain CT scan of the skull showed that the left side of the brain had high density shadows with uneven lamellae and unclear borders, and scattered internal calcification points. The enhancement is seen as irregular enhancement, the boundary is still unclear, and thick stripe blood vessels can be seen around it. After a delay of 5 minutes, you can see that the density of the enhanced area is weakened. After 8 years, the above symptoms were re-admitted to the hospital. MRI scan showed that there was an irregular abnormal signal in the left cerebral foot and the middle and lower part of the pontine, about 1.5cm × 1.5cm × 2.8cm in size. The T1 weighted phase showed a mixed signal of high and low, the T2 weighted phase showed a high signal in the center, and low signals in the surrounding area. No obvious occupying effect was seen, arteriovenous blood vessels were well developed, and no obvious blood supply arteries and drainage veins were found in the lesion area, which showed cavernous hemangioma of the midbrain and pontine.

  Case 3

  The patient was male, 8 years old. The family found that their eyes were dazed, and they could not move from side to side. On the third day, I ate cyanosis, staggered and stumbled, and fell easily. On the fifth day, I found horizontal and vertical nystagmus in my eyes, weak bilateral abduction, weakness in the right facial muscles and trapezius, and bilateral soft palate. Lifting power is weak, cyanosis is swallowed, articulation is difficult, pronunciation is unclear, tongue extension is to the right, no muscle atrophy. Both lower extremities tendon reflexes are active, double Babinski's sign is positive, active movement of the limbs is difficult, right side is, no sensory disturbance and meningeal irritation sign. After two months, symptoms gradually worsened, and bilateral paralysis and quadriplegia were more pronounced. No obvious signs of increased intracranial pressure. There were no abnormalities in the head and lateral position and the skull base radiograph. Cerebrospinal fluid was normal and died after three months. In this case, postmortem examination revealed a pathological diagnosis of pleomorphic glioblastoma in the brainstem. The lesions were mainly pontine, involving both sides, involving the upper part of the cerebrum, and spreading to the vermicular cerebellum.