Rejected

A previously healthy, 10-years-old girl presented with progressively worsening pain and weakness of the limbs for the past 2 weeks. It initially started with low-grade fever lasting for 4 days followed by severe pain over bilateral lower and upper limbs. Gradually she became bed-ridden. On examination, she had severe neck rigidity, generalized tenderness all over the body, generalized hyperalgesia, hyporeflexia, bilateral extensor plantar response and toe-walking. An initial clinical diagnosis of Landry-Guillain Barry syndrome was considered. Nerve conduction study showed generalized, demyelinating polyneuropathy. She was administered IVIG and was evaluated for other causes of arachnoiditis. MRI brain and spine showed enhancement and clumping of nerve roots in the conus and cauda equina. CECT chest showed necrotic mediastinal lymphnodes. A final diagnosis of disseminated tuberculosis with tuberculous arachnoiditis was considered and she was administered ATT, pulse methylprednisolone followed by maintenance oral corticosteroids. Currently, after 5 months of therapy, she has recovered clinically.

Idiopathic intracranial hypertension is a condition of raised intracranial pressure of unknown cause. Features include new onset headache, which is frequently non-specific; papilloedema is present, visual disturbances are common; and there may be sixth nerve palsy. Diagnosis includes brain imaging with venography to exclude structural causes and venous sinus thrombosis. Lumbar puncture reveals pressure greater than 250 mmCSF with normal constituents. Treatments aim to modify the disease, prevent permanent visual loss and manage headaches. These include weight loss. For those with rapid visual decline, urgent surgical intervention is essential. For most, this is a chronic condition characterised by significantly disabling headaches.

Muscle pain as a common symptom in daily practice frequently occurs as a non-specific accompanying symptom in multiple internal and neurological diseases. Primarily inflammatory or autoimmune muscular diseases are causing muscle pain. However, a number of non-inflammatory causes of pain can also be considered for differential diagnosis. These are presented in this article. In principle, a distinction must be made between focal and diffuse muscle pain. As an invasive diagnostic procedure, a muscle biopsy should only be performed as the last step in the diagnostic alogorithm. If diffuse muscle pain is only associated with slight muscle weakness or is completely absent, there is usually a primary rheumatic cause. Statins (HMG-CoA reductase inhibitors) can lead to rhabdomyolysis, muscle fiber atrophy and muscle necrosis by damaging the muscle fiber membrane. Myotonias are autosomal dominant or autosomal recessive inherited disorders of muscle function. The genetic defect leads to pronounced muscle stiffness. The cause of metabolic myopathies can be disorders of the carbohydrate, fat or purine metabolism. Fibromyalgia syndrome (FMS) is a non-inflammatory disease and, according to the current knowledge, recognized as the result of an exposure to physical, biological and psychosocial factors (biopsychological disease model). To help diagnosing FMS, pain regions and core symptoms (fatigue, sleep disturbances) can be detected using questionnaires (Widespread Pain Index [WPI] and Symptom Severity Scale [SSS]).

To compare analgesic efficacy and fetal effects between transdermal administration of fentanyl and IM administration of buprenorphine in pregnant sheep.

Dynapenic abdominal obesity (D/AO) has been associated with negative outcomes in older people, including trait of falls.

Although the sphenoidal emissary foramen (SEF) and its content are anatomically and clinically relevant, accurate description of them in the modern literature is lacking.

We report a case of deep femoral artery (DFA) retrograde access for recanalization of an accidental ostial occlusion complicating an antegrade-retrograde superficial femoral artery (SFA) procedure. A 77-year-old man with chronic limb-threatening ischemia of the right lower limb was submitted to a duplex ultrasound which showed a heavy calcified SFA chronic total occlusion. During antegrade and retrograde attempts to cross the SFA obstruction, a control angiogram unexpectedly showed the ostial occlusion of DFA. Several antegrade attempts to cross the DFA occlusion with various guidewires and catheters were unsuccessfully made. Retrograde access was achieved by direct puncture of the DFA distally to the first perforating artery. With sheathless approach the occlusion was crossed, the retrograde guidewire was externalized through the femoral sheath, and the balloon angioplasty was than antegradely performed. The SFA recanalization was interrupted because of patient discomfort. The patient had an uncomplicated recovery, with immediate resolution of rest pain probably due to the resolution of the underestimated DFA stenosis. The retrograde DFA access is a useful bailout technique in case of accidental ostial occlusion of DFA.

Wolff-Parkinson-White (WPW) syndrome is a rare disease that can cause various patterns of tachyarrhythmias. The main goal of anaesthesiologists for the perioperative anaesthetic management of WPW patients must be to avoid sympathetic stimulation and prevent tachyarrhythmias.

Cranial nerve (CN) VII palsy is a rare complication of neuraxial blockade. The likely etiology of the palsy is intracranial hypotension from cerebrospinal fluid loss leading to traction on CN VII. The presentation of symptoms of CN VII palsy from intracranial hypotension closely resembles a more common cause of CN VII injury, Bell's palsy, and the 2 can be difficult to differentiate. We present a patient who had a dural puncture with development of a headache and CN VII palsy, which improved with epidural blood patch (EBP). EBP should be considered for patients with suspected CN palsy from intracranial hypotension.

Intracranial tuberculomas are rare yet lethal forms of tuberculosis. Diagnosis is often difficult because of its nonspecific symptoms and radiological findings.