China
Africa
Explore chapters and articles related to this topic
Dementia
Published in Henry J. Woodford, Essential Geriatrics, 2022
The frontal release signs are neurological phenomena that originate from the brainstem or below. These signs are present in newborn children until subcortical myelination is completed. They may recur in later life in healthy individuals or in association with cerebral damage.9 They are then termed ‘release' signs due to the loss of the cortical inhibition of the brainstem-mediated mechanisms. They have been detected in 55% of people with AD (mean age 68 years) compared to 9% of healthy control subjects (mean age 62).22 In general, their occurrence does not correlate well with cognitive function.Grasp reflex: the patient grasps an object that is stroked across their palm.Pout (snout) reflex: a pouting facial expression is produced when the area lateral to the upper lip is stroked.Glabellar tap: the area between the eyebrows is gently tapped (with the examiner's arm approaching from above/behind to prevent blinking to a threatening stimulus). A positive result is achieved when the patient continues to blink beyond the first three taps.
Assessment of Cognitive Impairment, Alzheimer’s Disease, and Other Forms of Dementia
Published in Gwen Yeo, Linda A. Gerdner, Dolores Gallagher-Thompson, Ethnicity and the Dementias, 2018
J. Wesson Ashford, Frederick A. Schmitt, Carr J. Smith, Vinod Kumar, Nusha Askari
Reflexes in the AD patient tend to be mildly brisk, an indication of cortical dysfunction. Though the snout reflex (pursing of lips elicited by light tapping of the closed lips near the midline) is frequently present in the normal elderly individual, it is invariably found in the AD patient and becomes more severe as the disease progresses. Other pathological reflexes are not typically seen in the mild AD patient and may be more indicative of frontal (palmomental, grasp) or Parkinsonian (glabellar) pathology.
Neurology: cranial nerves
Published in Shahed Yousaf, Medical Examination Made Memorable (MEMM), 2018
The facial nerve is the efferent limb of the corneal reflex (touching the cornea causes contraction of the orbicularis oculi and bilateral blinking), palmomental reflex (scratching the thenar eminence causes contraction of the ipsilateral mentalis muscle), pout or snout reflex (brisk tap on the lips causes bilateral pursing of the lips), nasopalpebral reflex (glabellar tap) and the efferent limb of the stapedius reflex.
Neurological Soft Signs in Cannabis Use Disorder with or without Psychosis: A Comparative Study from India
Published in Journal of Dual Diagnosis, 2021
Arpit Parmar, Rakesh Lal, Siddharth Sarkar, Yatan Pal Singh Balhara
The Neurological Evaluation Scale (NES) is the most widely used tool to assess neurological soft signs in psychiatry research (Buchanan & Heinrichs, 1989). NES includes 26 items, of which 14 are rated separately on the right and left sides. The items are clustered into three subdomains: motor coordination, sequencing of motor tasks, and sensory integration. Rest items are lumped together under the rubric of “others”. The motor coordination subdomain includes tandem walk, rapid alternating movements, finger-thumb opposition, and finger-nose test. The sensory subdomain includes items such as audio-visual integration, stereognosis, graphesthesia, extinction, and right/left confusion. Sequencing of motor tasks includes tests such as fist-ring test, fist-edge-palm test, rhythm tapping test, and Ozeretski test. Other items include adventitious overflow test, Romberg test, tremors, memory, mirror movements test, synkinesis, convergence, gaze impersistence, Glabellar reflex, Snout reflex, Grasp reflex, and Suck reflex. The intraclass correlations ranged from 0.71 (motor coordination subscale) to 0.95 (total score) (Bombin et al., 2003; Buchanan & Heinrichs, 1989). The NES scale's interrater reliability ranges from 0.72 to 0.98, with a kappa value of 0.91 for the total score. The scale was applied in all three groups.
The first case of the TARDBP p.G294V mutation in a homozygous state: is a single pathogenic allele sufficient to cause ALS?
Published in Amyotrophic Lateral Sclerosis and Frontotemporal Degeneration, 2020
Lucia Corrado, Viviana Pensato, Roberta Croce, Alice Di Pierro, Simona Mellone, Eleonora Dalla Bella, Ettore Salsano, Elvezia Maria Paraboschi, Mara Giordano, Massimo Saraceno, Letizia Mazzini, Cinzia Gellera, Sandra D’Alfonso
The proband (#10402) is a 44-year-old male of Moroccan origin, with a family history of ALS (his brother died at age 47 of ALS). He showed first clinical signs at the age of 43 with progressive weakness of the right hand and dysarthria. During the disease course, the patient experienced progressive weight loss and worsening of the weakness of the right upper limb. One year after the onset he was examined by a neurologist in Morocco who reported dysarthria, fasciculation of tongue and muscular diffused hypotrophy, particularly of the right hand. EMG demonstrated diffuse denervation whereas brain MRI was normal. The serum creatine kinase value was slightly increased (400 U/L). A diagnosis of Suspected Motoneuron Disease was made with an ALS-FRS-R score of 41. Two years after symptoms onset, the patient was visited for the first time to our tertiary ALS Center. At the time of our first examination he presented with dysphagia and need of dietary consistence changes, severe dysarthria, signs of frontal liberation (snout reflex), tongue’s hypotrophy, proximal and distal muscular hypotrophy, hyperreflexia of upper and lower limbs with large fasciculations and exertional muscle cramps. At the MRC scale we found a severe weakness (2/5) of distal muscles of the upper limbs (particularly in the right part), and a moderate weakness (4/5) of the distal muscles of the lower limbs. ALS FRS-R score was 35. Respiratory function was normal (FVC 93%, FEV1 112%, FEV1/FVC ratio 123%, DLCO 122%, arterial oxygen saturation 97%). A standardized neuropsychological assessment was impossible because of language barriers but no cognitive or behavioral symptoms were reported by the patient and the family. No further clinical data are available because the patient refused follow-up visits.