76 Sentences With "palsies" | Random Sentence Generator

And then there's hereditary neuropathy with liability to pressure palsies (HNPP), a genetic condition that makes people more susceptible to nerve compression injuries.

Comedian Zach Anner takes readers on his wild wheelchair ride through 30 amazing years of dealing with cerebral palsy – "the sexiest of the palsies," as he likes to say – in his new memoir If at Birth You Don't Succeed: My Adventures with Disaster and Destiny.

Isolated sixth nerve palsies in children are assumed to be due to brain tumors until proven otherwise.

Clinical signs include: unilateral upper motor neuron limb weakness, cerebellar signs, and cranial nerve palsies (VI, VII nerve palsies and bulbar palsy). Some cases presented with flaccid paralysis alone. In northern Australia, all melioidosis with encephalomyelitis cases had elevated white cells in the cerebrospinal fluid (CSF), mostly mononuclear cells with elevated CSF protein.

To compensate for this, patients with trochlear nerve palsies tilt their heads to the opposite side, in order to fuse the two images into a single visual field. The characteristic appearance of patients with fourth nerve palsies (head tilted to one side, chin tucked in) suggests the diagnosis, but other causes must be ruled out. For example, torticollis can produce a similar appearance.

In Moebius-like syndrome, only one side of the face is affected, but with additional nerve palsies of the affected facial and abducens nerve.

Characteristic findings following injury will be as a result of radial nerve palsy (e.g. weakness of wrist/finger extension and sensory loss over the dorsum of the hand). The vast majority of radial nerve palsies occurring as a result of humeral shaft fractures are neurapraxias (nerve conduction block as a result of traction or compression of the nerve), these nerve palsies can be expected to recover over a period of months. A minority of palsies occur as a result of more significant axonotmeses (division of the axon but preservation of the nerve sheath) or the even more severe neurotmeses (division of the entire nerve structure).

In an anterior dislocation the limb is held by the person in externally rotated, extension and abduction. Femoral nerve palsies can be present, but are uncommon.

The VIth nerve's course is short and lesions in the orbit rarely give rise to isolated VIth nerve palsies, but more typically involve one or more of the other extraocular muscle groups.

While commonly affected by palsies of the inferior division of the oculomotor nerve, isolated palsies of the inferior oblique (without affecting other functions of the oculomotor nerve) are quite rare. "Overaction" of the inferior oblique muscle is a commonly observed component of childhood strabismus, particularly infantile esotropia and exotropia. Because true hyperinnervation is not usually present, this phenomenon is better termed "elevation in adduction". Surgical procedures of the inferior oblique include: loosening (also known as recession see Strabismus surgery), myectomy, marginal myotomy, and denervation and extirpation.

Oculomotor palsy can arise as a result of a number of different conditions. Non traumatic pupil-sparing oculomotor nerve palsies are often referred to as a 'medical third' with those affecting the pupil being known as a 'surgical third'.

Some data suggest that about 90% of Lyme facial palsies treated with antibiotics recover fully a median of 24 days after appearing and most of the rest recover with only mild abnormality. However, in Europe 41% of people treated for facial palsy had other lingering symptoms at followup up to 6 months later, including 28% with numbness or altered sensation and 14% with fatigue or concentration problems. Palsies in both sides of the face are associated with worse and longer time to recovery. Historical data suggests that untreated people with facial palsies recover at nearly the same rate, but 88% subsequently have Lyme arthritis. Other research shows that synkinesis (involuntary movement of a facial muscle when another one is voluntarily moved) can become evident only 6–12 months after facial palsy appears to be resolved, as damaged nerves regrow and sometimes connect to incorrect muscles.

Oil of brick was used in pre-modern medicine as a treatment for tumors, in the spleen, in palsies, and epilepsies. It was used by lapidaries as a vehicle for the emery by which stones and gems were sawn or cut.

The skin and hair may be sensitive to touch. Cranial nerve palsies and optic neuritis are uncommon. The acute uveitic phase occurs a few days later and typically lasts for several weeks. This phase is heralded by bilateral panuveitis causing blurring of vision.

Tolosa–Hunt syndrome (THS) is a rare disorder characterized by severe and unilateral headaches with orbital pain, along with weakness and paralysis (ophthalmoplegia) of certain eye muscles (extraocular palsies). In 2004, the International Headache Society provided a definition of the diagnostic criteria which included granuloma.

Other common signs and symptoms include: Ptosis, chemosis, cranial nerve palsies (III, IV, V, VI). Sixth nerve palsy is the most common. Sensory deficits of the ophthalmic and maxillary branch of the fifth nerve are common. Periorbital sensory loss and impaired corneal reflex may be noted.

The hallmark of malignant otitis externa (MOE) is unrelenting pain that interferes with sleep and persists even after swelling of the external ear canal may have resolved with topical antibiotic treatment. It can also cause skull base osteomyelitis (SBO), manifested by multiple cranial nerve palsies, described below under the "Treatment" heading.

Ruben, M. (2017, November). Conjugate Gaze Palsies - Neurologic Disorders. Retrieved from Internuclear ophthalmoplegia: Internuclear ophthalmoplegia affects horizontal gaze, such that one eye is capable of full horizontal movement, while the other is incapable of gazing in the direction contralateral to the affected eye.Toral, M., Haugsdal, J., & Wall, M. (2017, June 08).

Syringobulbia is a medical condition in which syrinxes, or fluid-filled cavities, affect the brainstem. This defect normally results from congenital abnormality, trauma or tumor growth. It mostly occurs within the lower brainstem as a slit-like gap. This may affect one or more cranial nerves, resulting in various kinds of facial palsies.

If the individual had only one copy of the PMP22 gene, on the other hand, the result was a clinically different heredity neuropathy with liability to pressure palsies. The differences in gene dosage created vastly different disease phenotypes which revealed the significant role that structural variation has on phenotype and susceptibility to disease.

Rare causes of isolated sixth nerve damage include Wernicke–Korsakoff syndrome and Tolosa–Hunt syndrome. Wernicke–Korsakoff syndrome is caused by thiamine deficiency, classically due to alcoholism. The characteristic ocular abnormalities are nystagmus and lateral rectus weakness. Tolosa-Hunt syndrome is an idiopathic granulomatous disease that causes painful oculomotor (especially sixth nerve) palsies.

As the VIth nerve passes through the subarachnoid space it lies adjacent to anterior inferior and posterior inferior cerebellar and basilar arteries and is therefore vulnerable to compression against the clivus. Typically palsies caused in this way will be associated with signs and symptoms of headache and/or a rise in ICP.

GAE starts slowly, with symptoms like headache, nausea, dizziness, irritability and a low-grade fever. The CNS symptoms depend on the part of the brain that is infected. Changes in behavior are an important sign. Other CNS signs may include seizures, focal neurologic signs, diplopia (double vision), cranial nerve palsies, ataxia, confusion, and personality changes.

The cause of congenital fourth nerve palsy is unclear in most cases. It may be neurogenic in origin, due to a dysgenesis of the CN IV nucleus or nerve, but a clinically similar palsy may result from absence or mechanical dysfunction (e.g., abnormal laxity) of the superior oblique tendon. Usually unilateral, congenital fourth nerve palsies can also occur bilaterally.

Many LCRs are concentrated in "hotspots", such as the 17p11-12 region, 27% of which is composed of LCR sequence. NAHR and non-homologous end joining (NHEJ) within this region are responsible for a wide range of disorders, including Charcot–Marie–Tooth syndrome type 1A, hereditary neuropathy with liability to pressure palsies, Smith–Magenis syndrome, and Potocki–Lupski syndrome.

The dead tissue forms a thick, gray coating that can build up in the throat or nose. This thick gray coating is called a "pseudomembrane". It can cover tissues in the nose, tonsils, voice box, and throat, making it very hard to breathe and swallow. Symptoms can also include cardiac arrhythmias, myocarditis, and cranial and peripheral nerve palsies.

The toxin is also useful in other cranial nerve palsies affecting eye muscles. Residual misalignments that remain following traditional strabismus surgery can be corrected with toxin injection. Toxin injections are used for temporary relief during the acute phase of thyroid ophthalmopathy, when misalignments are too unstable to treat surgically. Botulinum toxin has also been used intraoperatively to augment a surgical effect.

Mientus has a rare neurological disorder called HNPP (Hereditary Neuropathy with Pressure Palsies). During his freshman ballet class at the University of Michigan, his foot went numb and he had to pull out of the class for the remainder of the year. He was then put in a stage tech class, where he met fellow actor Darren Criss. Mientus is openly bisexual.

Because diazinon is fat soluble, there is potential for delayed toxicity if significant amounts of diazinon are stored in fatty tissues. Intermediate syndrome generally occurs within 24-96 hours after exposure. Intermediate syndrome in humans is characterized by difficulty breathing and muscular weakness, often in the face, neck and proximal limb muscles. Cranial nerve palsies and depressed tendon reflexes have also been reported.

The use of birth control pills does not affect the risk. Types of work that are associated include computer work, work with vibrating tools and work that requires a strong grip. Trauma may also place a role, as may genetics. Carpal tunnel is a feature of a form of Charcot-Marie-Tooth syndrome type 1 called hereditary neuropathy with susceptibility to pressure palsies.

Control of movement is limited at birth, and purposeful voluntary movements develop all the way until puberty.Stanley, Fiona et al. "Cerebral Palsies: Epidemiology and Causal Pathways", page 48 (2000 Cambridge University Press): "Motor competence at birth is limited in the human neonate. The voluntary control of movement develops and matures during a prolonged period up to puberty...."Becher, Julie-Claire.

In more than half of cases, normal activity is limited by significant fatigue and pain. Infrequently, inflammation of the eyes may occur in the form of iridocyclitis, or uveitis, and retinal lesions may occur. Temporary damage to the liver may occur. Rarely, neurological disorders have been reported in association with Chikungunya virus, including Guillain–Barré syndrome, palsies, meningoencephalitis, flaccid paralysis and neuropathy.

People affected by Powassan virus generally first show symptoms 1 to 3 weeks after infection. The initial symptoms include fever, headache, nausea, occasional confusion, and weakness. With severe Powassan illnesses the victims should be hospitalized, because the symptoms do worsen. If not treated, symptoms could extend to meningoencephalitis, which may include: seizures, aphasia, cranial nerve palsies, paresis and altered mental status.

The most common cause of chronic fourth nerve palsy is a congenital defect, in which the development of the fourth nerve (or its nucleus) is abnormal or incomplete. Congenital defects may be noticed in childhood, but minor defects may not become evident until adult life, when compensatory mechanisms begin to fail. Congenital fourth nerve palsies are amenable to surgical treatment.

Zoster ophthalmicus occurs in approximately 10% to 25% of cases. In some people, symptoms may include conjunctivitis, keratitis, uveitis, and optic nerve palsies that can sometimes cause chronic ocular inflammation, loss of vision, and debilitating pain. Shingles oticus, also known as Ramsay Hunt syndrome type II, involves the ear. It is thought to result from the virus spreading from the facial nerve to the vestibulocochlear nerve.

Recovery was judged moderate in 12% and poor in only 4% of patients. quoted in Another study found that incomplete palsies disappear entirely, nearly always in the course of one month. The patients who regain movement within the first two weeks nearly always remit entirely. When remission does not occur until the third week or later, a significantly greater part of the patients develop sequelae.

The headache is worse on coughing, sneezing or bending and progressively worsens over time. There may also be personality or behavioral changes. In addition to the above, if mass effect is present with resulting displacement of brain tissue, additional signs may include pupillary dilatation, abducens palsies, and the Cushing's triad. Cushing's triad involves an increased systolic blood pressure, a widened pulse pressure, bradycardia, and an abnormal respiratory pattern.

Hereditary neuropathy with liability to pressure palsy (HNPP) is a peripheral neuropathy, a condition that affects the nerves.update 2014 Pressure on the nerves can cause tingling sensations, numbness, pain, weakness, muscle atrophy and even paralysis of the affected area. In normal individuals, these symptoms disappear quickly, but in sufferers of HNPP even a short period of pressure can cause the symptoms to occur. Palsies can last from minutes or days to weeks or even months.

Under reported complications include myelitis, Guillain–Barré-type syndrome, cranial nerve palsies, transient or permanent hydrocephalus, sensorineural hearing loss, orchitis, arthritis and parotitis. LCMV infections have also been associated with pancreatitis, pneumonitis, myocarditis and pericarditis. The entire illness usually lasts 1 to 3 weeks, nonetheless, temporary or permanent neurological damage is possible in all central nervous system infections, especially in cases of meningoencephalitis. Chronic infections have not been reported in humans and deaths rarely occur.

In brachial plexus avulsions, the brachial plexus (a bundle of nerves that communicates signals between the spine and the arms, shoulders, and hands) is torn from its attachment to the spinal cord. One common cause of brachial plexus avulsions is when a baby's shoulders rotate in the birth canal during delivery, which causes the brachial plexus to stretch and tear.National Institute of Neurological Disorders and Stroke. NINDS Erb-Duchenne and Dejerine-Klumpke Palsies Information Page.

CNS symptoms begin with mild cognitive impairment and slowed reactions, and in a very severe form often progress to unconsciousness. Patients may present with neuropathic pain early in the infection. Eventually, severe infection will lead to ascending weakness, quadriparesis, areflexia, respiratory failure, and muscle atrophy, and will lead to death if not treated. Occasionally patients present with cranial nerve palsies, usually in nerves 7 and 8, and rarely larvae will enter ocular structures.

Disorders of conjugate gaze typically consist of the inability to move one or both eyes in the desired direction, or the inability to prevent eyes from making vergence movements. Conjugate gaze palsy: Conjugate gaze palsies typically affect horizontal gaze, although some affect upward gaze. Few affect downward gaze. These effects can range in severity from a complete lack of voluntary eye movement to mild impairments in speed, accuracy or range of eye movement.

An example of ragged red fibers A neuro-ophthalmologist is usually involved in the diagnosis and management of KSS. An individual should be suspected of having KSS based upon clinical exam findings. Suspicion for myopathies should be increased in patients whose ophthalmoplegia does not match a particular set of cranial nerve palsies (oculomotor nerve palsy, fourth nerve palsy, sixth nerve palsy). Initially, imaging studies are often performed to rule out more common pathologies.

The first aims of management should be to identify and treat the cause of the condition, where this is possible, and to relieve the patient's symptoms, where present. In children, who rarely appreciate diplopia, the aim will be to maintain binocular vision and, thus, promote proper visual development. Thereafter, a period of observation of around 6 months is appropriate before any further intervention, as some palsies will recover without the need for surgery.

The involvement of the peripheral or central nervous system is relatively rare and only occurs in 3% of persons affected with RP, and is sometimes seen in a relation with concomitant vasculitis. The most common neurological manifestation are palsies of the cranial nerves V and VII. Also hemiplegia, ataxia, myelitis and polyneuropathy have been reported in scientific literature. Very rare neurological manifestations include aseptic meningitis, meningoencephalitis, stroke, focal or generalized seizures and intracranial aneurysm.

The origins of the vast majority of congenital oculomotor palsies are unknown, or idiopathic to use the medical term. There is some evidence of a familial tendency to the condition, particularly to a partial palsy involving the superior division of the nerve with an autosomal recessive inheritance. The condition can also result from aplasia or hypoplasia of one or more of the muscles supplied by the oculomotor nerve. It can also occur as a consequence of severe birth trauma.

This nuclear gene, COX10, encodes heme A: farnesyltransferase, which is not a structural subunit but required for the expression of functional COX and functions in the maturation of the heme A prosthetic group of COX. A gene mutation, which results in the substitution of a lysine for an asparagine (N204K), is identified to be responsible for cytochrome c oxidase deficiency. In addition, this gene is disrupted in patients with CMT1A (Charcot-Marie-Tooth type 1A) duplication and with HNPP (hereditary neuropathy with liability to pressure palsies) deletion.

In general, symptoms and signs that suggest a rise in ICP include headache, vomiting without nausea, ocular palsies, altered level of consciousness, back pain and papilledema. If papilledema is protracted, it may lead to visual disturbances, optic atrophy, and eventually blindness. The headache is classically a morning headache which may wake them from sleep. The brain is relatively poorly supplied by oxygen as a result of mild hypoventilation during the sleeping hours and also cerebral edema may worsen during the night due to the lying position.

Diplopia is also increased on looking to the affected side and is partly caused by overaction if the medial rectus on the unaffected side as it tries to provide the extra innervation to the affected lateral rectus. These two muscles are synergists or "yoke muscles" as both attempt to move the eye over to the left or right. The condition is commonly unilateral but can also occur bilaterally. The unilateral abducens nerve palsy is the most common of the isolated ocular motor nerve palsies.

BVVL is marked by a number of cranial nerve palsies, including those of the motor components involving the 7th and 9th-12th cranial nerves, spinal motor nerves, and upper motor neurons. Major features of BVVL include facial and neck weakness, fasciculation of the tongue, and neurological disorders from the cranial nerves. The neurological manifestations develop insidiously: they usually begin with sensorineural deafness, progress inexorably to paralysis, and often culminate in respiratory failure. Most mortality in patients has been from either respiratory infections or respiratory muscle paralysis.

Uveitis with poliosis of the eyelashes The disease is characterised by bilateral diffuse uveitis, with pain, redness and blurring of vision. The eye symptoms may be accompanied by a varying constellation of systemic symptoms, such as auditory (tinnitus, vertigo, and hypoacusis), neurological (meningismus, with malaise, fever, headache, nausea, abdominal pain, stiffness of the neck and back, or a combination of these factors; meningitis, CSF pleocytosis, cranial nerve palsies, hemiparesis, transverse myelitis and ciliary ganglionitis), and cutaneous manifestations, including poliosis, vitiligo, and alopecia. The vitiligo often is found at the sacral region.

Mutations in the COX10 gene can result in numerous clinical phenotypes, from tubulopathy and leukodystrophy to Leigh syndrome to fatal infantile cardiomyopathy to a French Canadian form of Leigh Syndrome. A wide variety of symptoms encompassing the entire range of COX deficiency symptoms have been reported, including ataxia, hypotonia, ptosis, lactic acidosis, proximal tubulopathy, anemia, myopathy, hypertrophic cardiomyopathy, sensorineural hearing loss, and leukodystrophy. In addition, this gene is disrupted in patients with CMT1A (Charcot-Marie-Tooth type 1A) duplication and with HNPP (hereditary neuropathy with liability to pressure palsies) deletion.

Multiple cranial nerve palsies can result, including the facial nerve (causing facial palsy), the recurrent laryngeal nerve (causing vocal cord paralysis), and the cochlear nerve (causing deafness). The infecting organism is almost always pseudomonas aeruginosa, but it can instead be fungal (aspergillus or mucor). MOE and SBO are not amenable to surgery, but exploratory surgery may facilitate the culture of unusual organism(s) that are not responding to empirically used anti-pseudomonal antibiotics (ciprofloxacin being the drug of choice). The usual surgical finding is diffuse cellulitis without localized abscess formation.

In 1750 Charleton published A Chemical Analysis of Bath Waters. The book describes a series of experiments to determine the mineral constituents of the thermal springs at Bath. The chemical system of Hermann Boerhaave was followed. He published a second tract An Inquiry into the Efficacy of Bath Waters in Palsies, and reprinted it in 1774, with his first publication and Tract the Third, containing Cases of Patients admitted into the Hospital at Bath under the care of the late Mr. Oliver, with some additional Cases and Notes.

Retinal venous dilation occurs in 59% of people with HACE. Rarer symptoms include brisk deep tendon reflexes, retinal hemorrhages, blurred vision, extension plantar reflexes, and ocular paralysis. Cranial nerve palsies occur in some unusual cases. In the bestselling 1996 non-fiction book Into Thin Air: A Personal Account of the Mt. Everest Disaster, Jon Krakauer describes the effects of HACE upon Dale Kruse, a forty-four-year-old dentist and one of the members of Scott Fischer's team: ‘Kruse was having an incredibly difficult time simply trying to dress himself.

The serious problems caused because of inflammation include headaches, seizures, vision problems, dizziness, behavior changes and even stroke. Severe lupus cerebritis symptoms include psychosis, dementia, peripheral neuropathy, cerebellar ataxia (failure of muscular coordination, usually on one side of the body), and chorea (jerky, involuntary movements). Stroke incidence is 3-20% in systemic lupus patients, and is highest in the first five years of the disease. Peripheral neuropathy (carpal tunnel syndrome, for example) occurs in more than 20% of systemic lupus patients and cranial nerve palsies occur in 10-15%.

At around this time, a German surgeon was also working on cerebral palsy, and distinguished it from polio. In the 1880s British neurologist William Gowers built on Little's work by linking paralysis in newborns to difficult births. He named the problem "birth palsy" and classified birth palsies into two types: peripheral and cerebral. Working in Pennsylvania in the 1880s, Canadian-born physician William Osler (18491919) reviewed dozens of CP cases to further classify the disorders by the site of the problems on the body and by the underlying cause.

When the eye is in the primary position (looking straight ahead), contraction of the superior oblique produces depression and intorsion in roughly equal amounts. To summarize, the actions of the superior oblique muscle are (1) depression of the eyeball, especially when the eye is adducted; and (2) intorsion of the eyeball, especially when the eye is abducted. The clinical consequences of weakness in the superior oblique (caused, for example, by fourth nerve palsies) are discussed below. This summary of the superior oblique muscle describes its most important functions.

Injury to the trochlear nerve cause weakness of downward eye movement with consequent vertical diplopia (double vision). The affected eye drifts upward relative to the normal eye, due to the unopposed actions of the remaining extraocular muscles. The patient sees two visual fields (one from each eye), separated vertically. To compensate for this, patients learn to tilt the head forward (tuck the chin in) in order to bring the fields back together—to fuse the two images into a single visual field. This accounts for the “dejected” appearance of patients with “pathetic nerve” palsies.

When the eye is in the primary position (looking straight ahead), contraction of the superior oblique produces depression and intorsion in roughly equal amounts. To summarize, the actions of the superior oblique muscle are (1) depression of the eyeball, especially when the eye is adducted; and (2) intorsion of the eyeball, especially when the eye is abducted. The clinical consequences of weakness in the superior oblique (caused, for example, by fourth nerve palsies) are discussed below. This summary of the superior oblique muscle describes its most important functions.

Harmful effects involving multiple organ failure and neurological impairment are difficult to treat, and can cause lifelong debilitation or be directly fatal. The central nervous system is often affected and results in various complications including cerebellitis, cranial nerve palsies, meningoencephalitis, plexopathy, transverse myelitis, and Guillan-Barré syndrome. Death rates due to complications can be up to 14% in brain infections, and 24% with multiple organ failure. In India, scrub typhus has become the major cause of acute encephalitis syndrome, which was earlier caused mainly by a viral infection, Japanese encephalitis.

Pamela took up a post as a research fellow in epidemiology to enable her to continue working whilst raising a family. She was a member of the UK national working party concerned with data recording in cerebral palsy research from 1985 to the early 1990s. She has published various papers in the field and was invited to deliver a paper at a UCLA conference ('Epidemiology of the Cerebral Palsies: a Foundation for Research and Prevention') in 1986. She developed the "Limb by Limb" method of data recording, a standardised methodology for clinicians providing data to epidemiologists.

GA1 can be described as a metabolic disorder, a neurometabolic disease, a cerebral palsy or a basal ganglia disorder (it is also misdiagnosed as shaken baby syndrome). Depending on the paradigm adopted, GA1 will mostly be managed with precursor restriction or with neurorehabilitation. So-called "orphan diseases", such as GA1, can be adopted into wider groups of diseases (such as carnitine deficiency diseases, cerebral palsies of diverse origins, basal ganglia disorders, and others); Morton at al. (2003b) emphasize that acute striatal necrosis is a distinctive pathologic feature of at least 20 other disorders of very different etiologies (e.g.

An injury to the axillary nerve normally occurs from a direct impact of some sort to the outer arm, though it can result from injuring a shoulder via dislocation or compression of the nerve. The axillary nerve comes from the posterior cord of the brachial plexus at the coracoid process and provides the motor function to the deltoid and teres minor muscles. An EMG can be useful in determining if there is an injury to the axillary nerve. The largest numbers of axillary nerve palsies arise due to stretch injuries which are caused by blunt trauma or iatrogenesis.

A gaze palsy is the paresis of conjugate eye movements. Horizontal gaze palsy may be caused by lesions in the cerebral hemispheres, which cause paresis of gaze away from the side of the lesion, or from brain stem lesions, which, if they occur below the crossing of the fibers from the frontal eye fields in the caudal midbrain, will cause weakness of gaze toward the side of the lesion. These will result in horizontal gaze deviations from unopposed action of the unaffected extraocular muscles. Another way to remember this is that patients with hemisphere lesions look towards their lesion, while patients with pontine gaze palsies look away from their lesions.

Indirect damage to the sixth nerve can be caused by any process (brain tumor, hydrocephalus, pseudotumor cerebri, hemorrhage, edema) that exerts downward pressure on the brainstem, causing the nerve to stretch along the clivus. This type of traction injury can affect either side first. A right-sided brain tumor can produce either a right-sided or a left-sided sixth nerve palsy as an initial sign. Thus a right-sided sixth nerve palsy does not necessarily imply a right-sided cause. Sixth nerve palsies are infamous as “false localizing signs.” Neurological signs are described as “false localizing” if they reflect dysfunction distant or remote from the expected anatomical location of pathology.

Synkinesis is associated with corticosteroid use. In longer-term follow-up, 16–23% of Lyme facial palsies do not fully recover. In Europe, about a quarter of people with Bannwarth syndrome (Lyme radiculopathy and lymphocytic meningitis) treated with intravenous ceftriaxone for 14 days an average of 30 days after first symptoms had to be retreated 3–6 months later because of unsatisfactory clinical response or continued objective markers of infection in cerebrospinal fluid; after 12 months, 64% recovered fully, 31% had nondisabling mild or infrequent symptoms that did not require regular use of analgesics, and 5% had symptoms that were disabling or required substantial use of analgesics.

The novel's title refers to a line from one of John Donne's epigraphs: > His mercies hath applied His judgments, and hath shaked the house, this > body, with agues and palsies, and set this house on fire with fevers and > calentures, and frightened the master of the house, which is my soul, with > horrors, and heavy apprehensions, and so made an entrance into me. This epigraph describes the basic theme of the novel: a troubled soul, the alcoholic Cass, is badly shaken by the "fire" of an encounter with evil, in the form of the aristocratic Mason Flagg. Ultimately, Cass' experiences with Flagg provide Cass with the inspiration he needs to redeem himself.

Athetoid cerebral palsy, or dyskinetic cerebral palsy (sometimes abbreviated ADCP), is a type of cerebral palsy primarily associated with damage, like other forms of CP, to the basal ganglia in the form of lesions that occur during brain development due to bilirubin encephalopathy and hypoxic–ischemic brain injury. Unlike spastic or ataxic cerebral palsies, ADCP is characterized by both hypertonia and hypotonia, due to the affected individual's inability to control muscle tone. Clinical diagnosis of ADCP typically occurs within 18 months of birth and is primarily based upon motor function and neuroimaging techniques. While there are no cures for ADCP, some drug therapies as well as speech, occupational therapy, and physical therapy have shown capacity for treating the symptoms.

The renowned British obstetrician William Smellie is credited with the first medical description of an obstetric brachial plexus palsy. In his 1768 treatise on midwifery, he reported a case of transient bilateral arm paralysis in a newborn after difficult labour. In 1861, Guillaume Benjamin Amand Duchenne coined the term "obstetric palsy of the brachial plexus" after analyzing four infants with paralysis of identical muscles in the arm and shoulder, after publishing his initial findings in 1855. In 1874, Wilhelm Heinrich Erb concluded in his thesis on adult brachial plexus injuries that associated palsies of the deltoid, biceps and subscapularis are derived from a radicular lesion at the level of C5 and C6 rather than isolated peripheral nerve lesions.

Pure granulomatous lesions are rare in patients with AIDS and other related immunodeficiency states, as the patients do not have adequate numbers of CD+ve T-cells to mount a granulomatous response to Acanthamoeba infection in CNS and other organs and tissues. A perivascular cuffing with amoebae in necrotic tissue is usual finding in the AIDS and related T-cell immunodeficiency conditions. Brain biopsy normally reveals severe oedema and hemorrhagic necrosis. A patient who has contracted this illness usually displays subacute symptoms, including altered mental status, headaches, fever, neck stiffness, seizures, and focal neurological signs (such as cranial nerve palsies and coma), all leading to death within one week to several months.

Patients sometimes adopt a face turned towards the side of the affected eye, moving the eye away from the field of action of the affected lateral rectus muscle, with the aim of controlling diplopia and maintaining binocular vision. Diplopia is typically experienced by adults with VI nerve palsies, but children with the condition may not experience diplopia due to suppression. The neuroplasticity present in childhood allows the child to 'switch off' the information coming from one eye, thus relieving any diplopic symptoms. Whilst this is a positive adaptation in the short term, in the long term it can lead to a lack of appropriate development of the visual cortex giving rise to permanent visual loss in the suppressed eye; a condition known as amblyopia.

The condition was initially described by Dr. James Paget. In a paper published in 1877, Paget told of five patients with "a rare disease of bones" which presented with slowly progressive bone deformities in the 4th and 5th decades of age. Strikingly, the first patient was described to have many of the classic complications of the disease, including arthritis related to abnormal bone mechanics, cranial nerve palsies associated with an enlarging skull, and malignant transformation of a tumor of the radius which ultimately proved fatal. Paget's post-mortem autopsy evaluation showed "bones of the vault of this skull were in every part increased to about four times the normal thickness," and microscopic evaluation showed evidence of both bone erosion and abnormal remodeling.

Fetal movements at the end of first trimester (early fetal stage) detected by 3D ultrasound The parts of the fetal brain that control movement will not fully form until late in the second trimester, and the first part of the third trimester.The development of cerebral connections during the first 20–45 weeks’ gestation. Seminars in Fetal and Neonatal Medicine, Volume 11, Issue 6, Pages 415-422 Control of movement is limited at birth, and purposeful voluntary movements develop during the long period up until puberty.Stanley, Fiona et al. "Cerebral Palsies: Epidemiology and Causal Pathways", page 48 (2000 Cambridge University Press). According to an overview produced by the Royal College of Physicians of Edinburgh, purposive movement begins at about 18 weeks, gradually replacing reflex movements, and purposeful voluntary movements then develop further after birth.

This group of diseases can further be difficult to distinguish early on in the disease process due to these general symptoms in addition to most people (reported around 75%) not realizing they have been bitten or exposed to the tick vector. Unique to early Lyme disease is the development of the classic erythema migrans skin rash, also known as the “bull’s eye” or “target” rash, which occurs in about 80% of people diagnosed with Lyme disease. This symptom can be an important distinguishing factor helping to make the diagnosis early. If Lyme disease is unrecognized, misdiagnosed, or improperly treated it can lead to much more severe and serious consequences with the spread of the spirochete to joints, heart, and nervous system causing arthritis, carditis, cranial nerve palsies or encephalopathy and cognitive dysfunction.

A cat, when seized with that distemper, springs like lightning through every corner of the house, falls into convulsions and dies. A dog falls into strong convulsions also but sometimes recovers. A cow grows perfectly mad in an instant and must be immediately killed. Fortunately, this distemper does not affect the human species.Peterkin, 1799, pp.98-99. As Pennant had noted in 1772, the human counterpart of the animals' lead-brash was "mill-reek": :The miners and smelters are subject here, as in other places, to the lead distemper, or mill-reek, as it is called here; which brings on palsies, and sometimes madness, terminating in death in about ten days.Pennant (1774), p.130. However, because lead was attracting such high prices during the American and Napoleonic Wars, and the domestic construction boom,At its peak (1809) lead was selling at £32 per ton (approx £21,000 in 2015 per 1,000kg). Yet, by 1827 the price had slumped to £12 per ton — due to the removal of import dues on foreign lead, and the significant expansion of Spanish lead production, due to the re-emergence of Spanish trade following the end of the Peninsular War (Smout, 1962, pp.