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Gigaxonin is a cytoskeletal protein, which may be important in actin cytoskeletal interactions
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CV155 158 Visual-evoked potentials are unobtainable or have prolonged latencies
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Axonal swellings with spheroid bodies can be found on biopsies of peripheral nerves, muscle, skin, and conjunctiva155 158
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INFANTILE NEUROAXONAL DYSTROPHY Clinical Features
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Infantile neuroaxonal dystrophy presents in the rst or second year of life, with progressive psychomotor regression, visual loss, generalized hypotonia, and weakness155 158 Those children who eventually ambulate usually lose the ability to walk independently over time due to progressive weakness, spasticity, and ataxia Some affected children develop complex partial or generalized tonic clonic seizures Muscle stretch re exes are usually reduced Optic atrophy is apparent on fundoscopic examination
Molecular Genetics and Pathogenesis
The genetic defect associated with infantile neuroaxonal dystrophy has not been identi ed A de ciency is that the lysosomal enzyme -N -acetyl-galactosamide has been identi ed in some158 but not all patients with infantile neuroaxonal dystrophy156
Treatment
There is no speci c treatment
PORPHYRIA Clinical Features
Laboratory Features
MRI scans reveal cerebellar and cerebral atrophy, hyperintensity on T2-weighted images in the periventricular white matter and dentate nuclei, and hypointense T2 images in the globus pallidus and substantia nigra156 The optic chiasm is often thin Motor and sensory NCS reveal decreased amplitudes and mild-to-moderate slowing of
Porphyria is actually a group of inherited disorders caused by defects in heme biosynthesis There are three forms of porphyria that are associated with peripheral neuropathy as well as CNS abnormalities: acute intermittent porphyria (AIP), hereditary coprophyria (HCP), and variegate porphyria (VP) (Fig 10 9)13,159 166 The acute neurologic manifestations are quite similar;
Intermediates
Glycine + Succinyl CoA -Aminolevulinic Acid
H2N N H
Enzymes
-Aminolevulinic Acid Synthase -Aminolevulinic Acid Dehydratase Porphobilinogen Deaminase Uroporphyrinogen III Cosynthase Uroporphyrinogen Decarboxylase Coproporphyrinogen Oxidase Protoporphyrinogen Oxidase Ferrichelatase
Diseases
HOOC
COOH
Sideroblastic Anemia (X-Linked) ALAD-Deficient Porphyria Acute Intermittent Porphyria Congenital Erythropoietic Porphyria Porphyria Cutanea Tarda Hereditary Coproporphyria Variegate Porphyria Erythropoietic Protoporphyria
Porphobilinogen Hydroxymethylbilane
(nonenzymatic)
Uroporphyrinogen I Coproporphyrinogen I
Uroporphyrinogen III Coproporphyrinogen III Protoporphyrinogen IX
N HN
Protoporphyrin IX Fe2+ Heme
HOOC
COOH
Figure 10 9 Porphyria pathway Schematic representation of hepatic heme synthesis pathway Defects in speci c enzymes at various intermediate steps (boxes) controlling the synthesis of heme can lead to different clinical forms of porphyria All of the noted diseases (boxes) have the potential to result in a neuropathy except porphyria cutanea tarda
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OTHER HEREDITARY NEUROPATHIES
however, a photosensitive rash is seen with HCP and VP but not in AIP Attacks of porphyria can be precipitated by certain drugs (usually those metabolized by the P450 system), hormonal changes (eg, pregnancy and luteal phase of the menstrual cycle), and dietary restrictions An acute attack of porphyria is often heralded by acute abdominal pain Subsequently, patients may develop agitation, hallucinations, or seizures Several days later, back and leg pain followed by weakness can occur and may mimic Guillian Barr syndrome Motor ine volvement can be asymmetric, proximal, or distal and affect arms or legs preferentially Cranial nerves can also be affected, leading to facial weakness and dysphagia Sensory impairment may be dif cult to determine if the patient is encephalopathic Muscle stretch re exes are often reduced Autonomic dysfunction manifested by signs of sympathetic overactivity (eg, pupillary dilatation, tachycardia, and hypertension) is common Constipation, urinary retention, and incontinence can also be seen Recovery is usually good, provided treatment is instituted rapidly to prevent excessive amounts of axonal damage
deaminase de ciency, HCP is caused by defects in coproporhyrin oxidase, and VP is associated with protoporphyrinogen oxidase (Fig 10 9) The pathogenesis of the neuropathy is not completely understood The biochemical alterations in heme production may effect production of energy via affects on oxidative phosphorylation in the mitochondria The inability to detoxify various drugs in the liver may have secondary toxic effects on the nervous system Finally, some recent studies suggest that porphyrin precursor neurotoxicity may arise due to activation of transcription factors pivotal in regulating cell survival171,172
Treatment
Patients should be treated with hematin and glucose to reduce the accumulation of heme precursors Intravenous glucose is started at a rate of 10 20 g/h If there is no improvement within 24 hours, intravenous hematin 2 5 mg/kg/d for 3 14 days should be given This hematin dose can be infused over a 30 60-minute period Drugs that can precipitate the acute porphyric attack should be avoided
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