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Generally, diseases outlined within the ICD-10 codes G40-G47 within Chapter VI: Diseases of the nervous system should be included in this category. Subcategories This category has the following 4 subcategories, out of 4 total.
Paroxysmal sympathetic hyperactivity (PSH) is a syndrome that causes episodes of increased activity of the sympathetic nervous system. Hyperactivity of the sympathetic nervous system can manifest as increased heart rate, increased respiration, increased blood pressure, diaphoresis , and hyperthermia . [ 1 ]
Paroxysmal tachycardia is a form of tachycardia which begins and ends in an acute (or paroxysmal) manner. It is also known as Bouveret-Hoffmann syndrome. [ 1 ] [ 2 ] [ 3 ]
Paroxysmal nocturnal dyspnea is a common symptom of several heart conditions such as heart failure with preserved ejection fraction, in addition to asthma, chronic obstructive pulmonary disease, and sleep apnea. [8] Other symptoms that may be seen alongside paroxysmal nocturnal dyspnea are weakness, orthopnea, edema, fatigue, and dyspnea. [9]
Spontaneous osteonecrosis of the knee is the result of vascular arterial insufficiency to the medial femoral condyle of the knee resulting in necrosis and destruction of bone. It is often unilateral and can be associated with a meniscal tear .
Peroneal nerve is most commonly interrupted at the knee and possibly at the joint of hip and ankle. Most studies reported that about 30% of peroneal nerve palsy is followed from knee dislocations. [1] Peroneal nerve injury occurs when the knee is exposed to various stress. It occurs when the posterolateral corner structure of knee is injured.
A difference of greater than 10-15° indicates a positive test and likely injuries to the posterolateral knee. Next, repeat the test with the patient's knees flexed at 90°. Increased rotation at 90° indicates a combined PCL and posterolateral knee injury. If the rotation decreases compared to 30°, then an isolated PLC injury has occurred.
A suspected contributor to familial PED is a mutation in the GLUT1 gene, SLC2A1, which codes for the transporter GLUT1, a protein responsible for glucose entry across the blood–brain barrier. [5] It is not thought that the mutation causes a complete loss of function of the protein but rather only slightly reduces the transporter's activity. [ 8 ]