In 1982 Lewis et al reported a group of patients with a chronic asymmetrical sensorimotor neuropathy mostly affecting the arms with multifocal involvement of peripheral nerves. Also in 1982 Dyck "et al" reported a response to prednisolone to a condition they referred to as chronic inflammatory demyelinating polyradiculoneuropathy. Parry and Clarke in 1988 described a neuropathy which was later found to be associated with IgM autoantibodies directed against GM1 gangliosides. This latter condition was later termed multifocal motor neuropathy This distinction is important because multifocal motor neuropathy responds to intravenous globulin alone while chronic inflammatory demyelinating polyneuropathy responds to intravenous globulin, steroids and plasma exchanges. It has been suggested that multifocal motor neuropathy is distinct from chronic inflammatory demyelinating polyneuropathy and that Lewis-Summer syndrome is a distinct variant type of chronic inflammatory demyelinating polyneuropathy.

The Lewis-Summer form of this condition is considered a rare disease with only 50 cases reported up to 2004. A total of 90 cases had been reported by 2009

Chronic inflammatory demyelinating polyneuropathy, also known as Vidaurri's disease, is believed to be due to immune cells, which normally protect the body from foreign infection, incorrectly attacking the nerves in the body instead. As a result, the affected nerves fail to respond, or respond only weakly, and on occasion, inordinately, to stimuli, causing numbing, tingling, pain, progressive muscle weakness, loss of deep tendon reflexes (areflexia), fatigue, and abnormal sensations. The likelihood of progression of the disease is high.

CIDP is under-recognized and under-treated due to its heterogeneous presentation (both clinical and electrophysiological) and the limitations of clinical, serologic, and electrophysiologic diagnostic criteria. Despite these limitations, early diagnosis and treatment is important in preventing irreversible axonal loss and improving functional recovery.

Lack of awareness and treatment of CIDP is also due to limitations of clinical trials. Although there are stringent research criteria for selecting patients to clinical trials, there are no generally agreed-on clinical diagnostic criteria for CIDP due to its different presentations in symptoms and objective data. Application of the present research criteria to routine clinical practice often miss the diagnosis in a majority of patients, and patients are often left untreated despite progression of their disease.

Polyradiculoneuropathy describes a condition in which polyneuropathy and polyradiculopathy occur together. An example is Guillain–Barré syndrome.

Treatment with a single course of intravenous immunoglobulin (IVIG) infusions has been demonstrated to be a potentially effective treatment (reported to have caused prolonged remission in a case associated with systemic lupus (Systemic lupus erythematosus) ).

The American College of Rheumatology has outlined 19 syndromes that are seen in NPSLE. These syndromes encompass disorders of the central and peripheral nervous systems:

- Aseptic meningitis

- Cerebrovascular disease

- Demyelinating syndrome

- Headache

- Movement disorder

- Myelopathy

- Seizure disorders

- Acute confusional state

- Anxiety disorder

- Cognitive dysfunction

- Mood disorder

- Psychosis

- Acute inflammatory demyelinating polyradiculoneuropathy

- Autonomic disorder

- Mononeuropathy (single/multiplex)

- Myasthenia gravis

- Cranial neuropathy

- Plexopathy

- Polyneuropathy

Each of the 19 syndromes are also stand-alone diagnoses, which can occur with or without lupus.

The majority of cases involve the central nervous system (CNS), which consists of the brain and spinal cord. The CNS syndromes can be subcategorized as either focal or diffuse. The focal syndromes are neurological, while the diffuse syndromes are psychiatric in nature. The most common CNS syndromes are headache and mood disorder.

Though neuropsychiatric lupus is sometimes referred to as "CNS lupus", it can also affect the peripheral nervous system (PNS). Between 10-15% of people with NPSLE have PNS involvement. Mononeuropathy and polyneuropathy are the most common PNS syndromes.

There are several possible mechanisms that underlie the nervous system manifestations of lupus. Specific syndromes may be vasculopathic, autoantibody-mediated, or inflammatory in nature.

There is evidence that the blood–brain barrier, which protects the central nervous system, is compromised in patients with NPSLE. As a result of this, autoantibodies are able to infiltrate the CNS and cause damage.

Sinus tachycardia is usually a response to normal physiological situations, such as exercise and an increased sympathetic tone with increased catecholamine release—stress, fright, flight, anger. Other causes include:

- Pain

- Fever

- Anxiety

- Dehydration

- Malignant hyperthermia

- Hypovolemia with hypotension and shock

- Anemia

- Heart failure

- Hyperthyroidism

- Mercury poisoning

- Kawasaki disease

- Pheochromocytoma

- Sepsis

- Pulmonary embolism

- Acute coronary ischemia and myocardial infarction

- Chronic obstructive pulmonary disease

- Hypoxia

- Intake of stimulants such as caffeine, theophylline, nicotine, cocaine, or amphetamines

- Hyperdynamic circulation

- Electric shock

- Drug withdrawal

- Porphyria

- Acute inflammatory demyelinating polyradiculoneuropathy

- Postural orthostatic tachycardia syndrome

Not required for physiologic sinus tachycardia. Underlying causes are treated if present.

Acute myocardial infarction. Sinus tachycardia can present in more than a third of the patients with AMI but this usually decreases over time. Patients with sustained sinus tachycardia reflects a larger infarct that are more anterior with prominent left ventricular dysfunction, associated with high mortality and morbidity. Tachycardia in the presence of AMI can reduce coronary blood flow and increase myocardial oxygen demand, aggravating the situation. Beta blockers can be used to slow the rate, but most patients are usually already treated with beta blockers as a routine regimen for AMI.

Practically, many studies showed that there is no need for any treatment.

IST and POTS. Beta blockers are useful if the cause is sympathetic overactivity. If the cause is due to decreased vagal activity, it is usually hard to treat and one may consider radiofrequency catheter ablation.