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The Nutrition-Focused History and Physical Examination (NFPE) in Malnutrition
Published in Michael M. Rothkopf, Jennifer C. Johnson, Optimizing Metabolic Status for the Hospitalized Patient, 2023
Michael M. Rothkopf, Jennifer C. Johnson
Look for hypo-reflexia, which may be due to low thiamine, hypercalcemia or hypermagnesemia. On the other hand, hyperreflexia can occur with hypocalcemia and hypomagnesemia. Disequilibrium, decreased vibration sense, frequent falls and decreased position sense are seen with B12 and copper deficiencies. Gait disturbance and ataxia may be another manifestation of thiamine, B12 and copper deficiencies.
Motor Neurological Examination of the Hand and Upper Limb
Published in J. Terrence Jose Jerome, Clinical Examination of the Hand, 2022
NINDS scale:Grade 0: Reflex absent: No evidence of contraction.Grade 1: Reflex small, less than normal; includes a trace response or a response brought out only with reinforcement: Decreased, but still present (hypo-reflexic). Hyporeflexia is generally associated with a lower motor neuron deficit (at the alpha motor neurons from spinal cord to muscle) e.g., Guillain–Barré syndrome.Grade 2: Reflex in the lower half of the normal range.Grade 3: Reflex in the upper half of the normal range: Super-normal (hyper-reflexic). Hyperreflexia is often attributed to upper motor neuron lesions e.g., multiple sclerosis.Grade 4: Reflex enhanced, more than normal; includes clonus if present, which optionally can be noted in an added verbal description of the reflex [7]. Clonus: Repetitive shortening of the muscle after a single stimulation.
Acute hypoxia and hyperventilation
Published in Nicholas Green, Steven Gaydos, Hutchison Ewan, Edward Nicol, Handbook of Aviation and Space Medicine, 2019
Nicholas Green, Steven Gaydos, Hutchison Ewan, Edward Nicol
Symptoms become apparent when PACO2 falls below 25 mmHg (3.3 kPa): Dizziness.Paraesthesia.Muscle contraction.Hyper-reflexia.Visual impairment – flashing lights and hallucinations.Unconsciousness (<15 mmHg, 2 kPa).
Decision-making and challenges within the evolving treatment algorithm in spinal muscular atrophy: a clinical perspective
Published in Expert Review of Neurotherapeutics, 2023
Lakshmi Balaji, Michelle A Farrar, Arlene M D’Silva, Didu S Kariyawasam
Ambiguous or subtle clinical findings may sometimes be apparent, denoting a prodromal period, or phenotransition from pre-symptomatic to clinically manifest, for affected individuals diagnosed through NBS [65]. For example, vascular dysautonomia, a rare finding that may precede weakness or areflexia, may be a clinical manifestation of SMA in neonates [70]. Hyper-reflexia may precede areflexia. Phenoconversion may be rapid for neonates with 2SMN2 copies, with a normal compound muscle action potential (CMAP) early on that precipitously drops and reaches a nadir within a few weeks [71]. Significantly, approximately 40% of those with 2SMN2 copies manifest symptoms of SMA within 6 postnatal weeks [67]. While this population has not been well studied within clinical trials, recent data has shown individuals with clinically manifest SMA diagnosed following NBS may achieve assisted or independent ambulation [67]. Compared to individuals with clinically based diagnoses and a longer latency to initiation of disease-modifying therapies, improved outcomes have been observed, suggesting a neuromuscular penumbra amenable to urgent therapy [67,72,73].
FDG-PET shows weak correlation between focal motor weakness and brain metabolic alterations in ALS
Published in Amyotrophic Lateral Sclerosis and Frontotemporal Degeneration, 2023
Stefan Sennfält, Marco Pagani, Fang Fang, Irina Savitcheva, Ulrika Estenberg, Caroline Ingre
The severity of motor symptoms (weakness) was documented in five separate areas: right upper extremity, left upper extremity, right lower extremity, left lower extremity, and in the bulbar area, using the following scoring system:0. No symptoms.1. Findings on clinical examination (e.g. hyperreflexia) but no effect on function.2. Slight effect on function (e.g. slight foot drop).3. Severe effect on function (e.g. considerable walking impairment).4. Complete paralysis.
A de novo c.113 T > C: p.L38R mutation of SPTLC1: case report of a girl with sporadic juvenile amyotrophic lateral sclerosis
Published in Amyotrophic Lateral Sclerosis and Frontotemporal Degeneration, 2022
Xiaoxuan Liu, Ji He, Weiyi Yu, Dongsheng Fan
A 12-year-old girl was referred with a history of lower limb spasticity manifesting as frequent falls and gait difficulties beginning at the age of 6. Her main neurodevelopmental milestones were normal. She was initially diagnosed with hereditary spastic paraplegia or JALS. Gradually, she had symmetrical weakness and atrophy of lower limbs, slowly progressive from distal to proximal. Her hand flexibility was also involved after 3 years of onset, with difficulty in writing. She also noticed mild atrophy in intrinsic muscle. No dysarthria and blurred speech were reported. The patient was born to nonconsanguineous healthy parents (38 and 40 years of age respectively). When she was first examined at age 10, she had moderate weakness of both proximal (with a Medical Research Council (MRC) rating of 4-/5) and distal (MRC 3/5) lower limbs. She had mild atrophy in both intrinsic hand muscles (Figure 1(A)) with MRC 5-/5. Hyperreflexia was found in the upper and lower limbs. Babinski and Hoffmann signs were absent. Sensory and cerebellar functions were normal.