Response Letter to Drs. Halperin and Greenberg
We thank Drs. Halperin and Greenberg for their interest in our recent article that provided a critical appraisal of what has been termed the mild axonal peripheral neuropathy of late neurologic Lyme disease [1 –3]. Dr. Halperin is correct that this entity was described in papers published over 20years ago [4–7]. Essentially, no recent articles have provided any new data affirming this entity in North America, but no systematic and rigorously conducted studies have been conducted to refute the existenc e of this entity in North America as well.
This article can educate those engaged in imaging of the nervous system and serve as a comprehensive tool in clinical cases.Key Points•Diagnostic criteria for LNB emphasise exclusion of an alternative cause to the clinical symptoms.•MRI makes a crucial contribution in the diagnosis and follow-up of LNB.•MRI may have normal findings, or show neuritis, meningitis, myelitis, encephalitis or vasculitis.•White matter lesions are not a prominent feature of LNB.
We report a case of difficult acute pain management in a patient with PTLDS who underwent dental extractions and required admission to an intensive care unit for pain control.
Discussionby Dr MGK Murthy, Dr GA PrasadChronic inflammatory demyelinating polyradiculoneuropathy (CIDP) is characterized clinically by a progressive or relapsing course of many months to years of symptoms similar to compressive myelopathy.Etiology Remains unknown, but T-cell activation in nerves plays an important role in the pathogenesis of CIDP&antigens in Schwann cells have been identified.PathologicallyCIDP is characterized by mononuclear cell infiltrates, edema, segmental demyelination, and remyelination&“onion bulb formation” which describes enlarged fascicles with increased endoneural connectiv...
Publication date: 2017 Source:Handbook of Clinical Neurology, Volume 145 Author(s): Istvan Katona, Joachim Weis This chapter reviews the diseases of the peripheral nerves from a neuropathologic point of view, with a special focus on specific morphologic changes, and includes a summary of the histopathologic methods available for their diagnosis. As the rate of obesity and the prevalence of type 2 diabetes increase, diabetic neuropathy is the most common cause of peripheral neuropathy. Many systemic disorders with metabolic origin, like amyloidosis, hepatic failure, vitamin deficiencies, uremia, lipid metabolism disorders,...
Conclusions:Our case demonstrates that rapidly progressive acute axonal polyneuropathy is a serious neurological manifestation of porphyria and if not diagnosed early, can lead to irreversible axonal injury and severe disability. This diagnosis should be considered in all cases of acute ascending weakness with minimal sensory deficits when electrodiagnostic features of demyelination are lacking.Disclosure: Dr. Sharma has nothing to disclose. Dr. Kumbham has nothing to disclose. Dr. Sahaya has nothing to disclose. Dr. Sasapu has nothing to disclose. Dr. Gundogdu has nothing to disclose.
Conclusions:Diagnostic approach to bilateral FNP should evaluate for: traumatic (skull fractures), infectious (classically Lyme disease), metabolic (diabetes), autoimmune (sarcoidosis, Guillain-Barré syndrome), congenital (Moebius syndrome) and neoplastic (brainstem tumors) entities. WM is a rare cause, a condition due to low-grade B cell lymphoma where lymphoplasmacytoid cells infiltrate different tissues and secrete monoclonal IgM. Peripheral neuropathy develops in 15–30% of the cases, usually a chronic, progressive, symmetric, predominantly distal polyneuropathy. Facial nerve impairment is unusual, caused b...
Conclusions:This case establishes the importance of clinical reasoning. Neurological exam suggested multilevel radiculopathy/plexopathy. Normal SNAPS argue against plexopathy, MRI, and CSF analysis confirmed the diagnosis of secondary CNS lymphoma invading the meninges and nerve roots.Disclosure: Dr. Datta has nothing to disclose. Dr. Roy has nothing to disclose. Dr. Meira Benchaya has nothing to disclose. Dr. Boland has nothing to disclose.
It can only be hoped that the paper by Wormser et al.(Wormser&Strle, 2016) can accomplish what a quarter century of deliberate neglect has not – the elimination of the concept of a symmetric diffuse axonal neuropathy as a distinct nosologic entity in Lyme disease. As the authors point out, this concept was introduced early in our understanding of Lyme disease –before 2 tier serologic testing - and included some patients diagnosed on th e basis of T cell testing – a procedure then advocated by one of Dr.
I read with great interest the article by Wormser et al. but found that many of the authors' stated reasons for questioning the existence and frequency of this type of Lyme neuropathy require critical appraisal themselves.
In older studies, a chronic distal symmetric sensory neuropathy was reported as a relatively common manifestation of late Lyme disease in the United States. However, the original papers describing this entity had notable inconsistencies and certain inexplicable findings, such as reports that this condition developed in patients despite prior antibiotic treatment known to be highly effective for other manifestations of Lyme disease. More recent literature suggests that this entity is seen rarely, if at all.