Pietro Emiliano Doneddu

Post-traumatic neuroma due to closed nerve injury. Is recovery after peripheral nerve trauma related to ultrasonographic neuroma size?

OBJECTIVE traumatic neuroma is a pathological condition of peripheral nervous system consisting of localized proliferation of injured nerve elements. The symptoms depend on the type of involved nerve (motor and/or sensitive) and on the site and the extension of the lesion. Ultrasound is the best tool to depict the morphology of nerve, especially in traumatic conditions. We present a study aimed to assess the correlation between the degree of nerve function and the ultrasound morphology of neuromas. PATIENTS AND METHODS we retrospectively evaluated 18 patients with neuromas (not transected) occurred after a closed nerve trauma evaluated with clinical and ultrasound assessment. The clinical evaluation was related to the % of increase of cross sectional area as detected by nerve ultrasound respect to normal nerve. RESULTS we observed that dimensions of neuromas are not related to function until neuroma have cross sectional area 5 times enlarged respect to normal nerve, in this case recovery never occurs. CONCLUSION our study failed to clear detect a relation between cross sectional area enlargement of neuroma and nerve function, but showed a cut off beyond which prognosis is negative. This result provide some useful information for prognosis, nevertheless we believe that future perspective studies are needed to better understand the timing of developing neuromas and its evolution.

Transfer to inpatient rehabilitation facilities after neurological admission

In recent years, much attention has been paid to concerns regarding prolonged length of stay (pLOS) and its economic and medical effects. Numerous studies suggest that pLOS leads to serious implications, such as delays in elective and urgent admissions, increased risk of adverse ward events—disability—mortality, increased rate of readmission and hospitalization, and increased costs [1, 2]. The causes and effects of this phenomenon in the neurological setting have not yet been studied extensively, and few studies present in literature are focused only on patients with stroke. A recent retrospective study showed that the delay in inpatient rehabilitation facility (IRF) placement was the most frequent cause of pLOS among patients with stroke [3]. Although concern has been raised that the capacity of existing IRFs may not be enough to meet the demands of an aging population, to our knowledge, the adequate number of IRFs units to deal with the need of a neurological department is still not defined in the literature. The aim of this study is to assess that number, on the basis of data obtained from our neurological Department (Policlinico ‘‘A. Gemelli’’, Institute of Neurology, a third level hospital in Rome, Lazio, Italy). We retrospectively studied all patients admitted to our Department of Neurology (general short-term ward and stroke unit) and transferred to IRFs after stabilization of the acute condition, during the 6-month period between 2014 July the 1st and 2014 December the 31st. Age, gender, diagnosis at discharge, and length of hospital stay were considered. pLOS was calculated for each patient as the number of days between last diagnostic test or consultation performed (chosen as indicator of possible transfer) and the actual date of transfer to IRFs. A total of 746 patients were admitted to our Department during the study period. Of these, 94 patients (12.6%) were transferred to IRFs. This group of 94 patients (54 males, 40 females, mean age 67 years, and ranged from 23 to 93 years) included 56 patients (60%) with stroke (10 of whom underwent thrombolytic therapy), 9 patients (9.5%) with encephalopathy/neurological infectious disease, 6 patients (6%) with myelopathy, 6 patients (6%) with peripheral neuropathy, 3 patients (3%) with myasthenia gravis, 3 patients (3%) with multiple sclerosis, 2 patients (2%) with Parkinson’s disease, 2 patients (2%) with epilepsy, 1 with amyotrophic lateral sclerosis, and 6 patients (6%) with other neurological conditions. Among these patients, three underwent percutaneous endoscopic gastrostomy, three underwent tracheostomy, and nine underwent central venous catheter insertion. According to the Italian National Healthcare System (INHS), 44 days of rehabilitation in IRFs are guaranteed as maximum treatment length. However, mean length of stay in IRFs is usually more and Regional Healthcare System (Lazio region) reimburses partially the additional time. Considering 44 days as the mean length of IRFs stay, the number of units required in IRFs to deal with the need of & Luca Padua luca.padua@unicatt.it

High-resolution ultrasound may depict pseudomeningocele

Pseudomeningocele is a pathological condition deriving from cerebrospinal fluid leak throughout a fissure of the dura mater. The came out fluid is enclosed in a space delimited by the soft tissues. It can be congenital, iatrogenic or traumatic (mainly in brachial plexus injury) and can be often associated with root avulsion, a severe condition which should be aware as soon as possible [1]. The incidence of traumatic pseudomeningocele of this type is 21–57 % [2, 3]. In brachial plexus injury, magnetic resonance (MR) is the gold standard to assess the damage, allowing the visualization of root avulsion and pseudomeningocele [3]. Even high-frequency ultrasound (US) may be used as first line tool in brachial plexus injury, showing data that, in some cases, require a comprehensive assessment through MR [4]. No cases of pseudomeningocele, visualized by US, have so far been reported. We describe two patients with traumatic brachial plexus injury, in whom US showed findings indicating the presence of fluid, close to a cervical root, compatible with pseudomeningocele. Case 1

Neuralgic amyotrophy mimicking Vernet syndrome

A 72-year-old Caucasian man, with a medical history of arterial hypertension, was admitted in our Neurology Department for acute pharyngodynia and extreme pain localized to the neck, right scalp and the ipsilateral ear canal, followed two days later by dysphagia and hoarseness. One week before he had suffered from a flu-like illness with fever. The pain resolved in 5 dayswhereas hoarseness and dysphagia persisted. At laryngoscopic examination right vocal-cord palsy was noted (Fig. 1). Neurological examination showed weakness of the right soft-palate with reduced gag-reflex and right shoulder ptosis with weakness (4/5 MRC) of right sternocleidomastoid and trapezius muscles. No fasciculation or scapular winging were noted. Sensory examination was unremarkable. Examination of the mouth and external auditory canal did not show any vescicular rash. Considering the unilateral involvement of IX, X and XI cranial nerves, the common causes of Vernet syndrome were investigated. Laboratory tests including blood count, serum-protein electrophoresis, immunofixation, C-reactive protein, creatine kinase, erythrocyte-sedimentation rate, TSH, FT3, FT4, antinuclear antibodies (ANA), extractable-nuclearantigens antibodies, antineutrophil-cytoplasmatic antibodies (ANCA), rheumatoid factor, antiganglioside antibodies, anti-AchR and antiMUSK antibodies, Lyme test, syphilis, varicella-zooster virus (VZV), Epstein–Barr virus (EBV), hepatitis A, B and C, and human immunodeficiency virus serologies (HIV) were normal. Cerebrospinal fluid analysis did not show any hyperproteinorrachia, pleocytosis or oligoclonal bands. PCR did not detect VZV or herpes simplex virus. Chest X-ray was negative. Brain and neck MR studies, CT scan of the basicranial region, and carotid ultrasonography failed to identify anymass or infiltrative lesion along the course of IX, X and XI cranial nerves. Nerve conduction studies and F-wave were normal. Electromyography exhibited fibrillation potentials and positive sharp-waves in the right trapezium, right sternocleidomastoid, deltoid muscles bilaterally, and in the left infraspinatus muscle. No abnormalities were noted in the cervical paraspinal muscles. Motor unit potentials were of normal configuration with reduced recruitment. Brachial plexus MR was normal. On the basis of the clinical history of intense pain followed two days later by weakness (dysphagia, hoarseness, right shoulder ptosis), considering the electromyographic pattern of mononeuritis multiplex and

Sleep palsy involving different nerves: Role of ultrasound

nosed with multiple isolated entrapment neuropathies instead, and surgical releases were recommended. Fortuitously, the patient later discovered that several family members had HNPP. With this information, a year following his initial presentation, genetic testing confirmed a deletion of PMP22 consistent with HNPP. Misdiagnosis of HNPP can be due to variable disease expression and difficulty in assessing family inheritance. Pain is traditionally not thought to be associated with HNPP. However, there have been reports of both neuropathic and musculoskeletal pain related to HNPP. Symptoms of pain may precede the more classic symptoms of transient paresthesias or weakness in HNPP. Of note, diagnosis may be delayed in patients who present with pain. Moreover, absence of family history should not preclude the diagnosis of HNPP. Approximately 20% of HNPP cases are sporadic due to de novo mutations in PMP22. In a large European collaborative study, 20% of the probands initially gave a negative family history, but with further investigation they were found to have a family history of HNPP. This case demonstrates that HNPP can present with musculoskeletal pain and further supports the heterogeneous phenotype of HNPP. In such cases, a comprehensive investigation with electrodiagnosis and molecular genetics is indicated. If multiple entrapment neuropathies are treated as isolated pathologies and HNPP is not recognized, patients may undergo needless or potentially harmful treatment. Surgical decompression in HNPP is controversial and is generally not recommended.

Cranial Nerve Involvement in Neuralgic Amyotrophy

Neuralgic Amyotrophy (NA) is generally conceived as a multifocal neuropathy of the brachial plexus. However, different atypical forms with the involvement of other peripheral nerves, such as the lumbosacral plexus, the intercostal and the phrenic nerve and the cranial nerves (CNs), have been reported in the literature. In an attempt to shed more light on the atypical presentation of NA with CN involvement, we summarized the most relevant features of all cases of idiopathic NA with CN palsy, published up to January 2016. CN involvement in NA usually occurs with concomitant classic brachial plexopathy. Less frequently, CN palsy is the unique manifestation of the syndrome. In these cases, clinical suspicion and imaging studies are essential for a correct diagnosis, which may have therapeutic and prognostic relevance.

Prolonged phone-call posture causes changes of ulnar motor nerve conduction across elbow

OBJECTIVE Postures and work-hobby activities may play a role in the origin and progression of ulnar neuropathy at the elbow (UNE), whose occurrence appears to be increasing. The time spent on mobile-phone has increased in the last decades leading to an increased time spent with flexed elbow (prolonged-phone-posture, PPP). We aimed to assess the effect of PPP both in patients with symptoms of UNE and in symptom-free subjects. METHODS Patients with pure sensory symptoms of UNE and negative neurophysiological tests (MIN-UNE) and symptom-free subjects were enrolled. We evaluated ulnar motor nerve conduction velocity across elbow at baseline and after 6, 9, 12, 15, and 18min of PPP in both groups. Fifty-six symptom-free subjects and fifty-eight patients were enrolled. Globally 186 ulnar nerves from 114 subjects were studied. RESULTS Conduction velocity of ulnar nerve across the elbow significantly changed over PPP time in patients with MIN-UNE, showing a different evolution between the two groups. CONCLUSIONS PPP causes a modification of ulnar nerve functionality in patients with MIN-UNE. SIGNIFICANCE PPP may cause transient stress of ulnar nerve at elbow.

Paradoxical Effect of Levetiracetam in Newly Diagnosed Type II Focal Cortical Dysplasia.

AbstractA paradoxical effect of antiepileptic drugs was defined as an increased seizure frequency or severity occurring shortly after introducing a drug considered effective for that kind of epilepsy. In addition, this effect should occur at nontoxic drug serum levels. So far, pathophysiological mechanisms underlying this phenomenon have not been clarified. Recent evidence suggests that the variability of drug effects may depend on precise intrinsic properties of dynamic networks involving the drug and its binding site. Although several reports of paradoxical seizure exacerbation have been reported for levetiracetam (LEV), a possible association with focal cortical dysplasia has never been described nor investigated. In this report, we document a paradoxical effect induced by LEV monotherapy in a patient with type II focal cortical dysplasia at LEV serum levels within the therapeutic range. A hint of pathophysiological hypothesis underlying this potential relationship will be also suggested.