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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.
Discussions (D)
Published in Terence R. Anthoney, Neuroanatomy and the Neurologic Exam, 2017
A second reason that some authors use the term “pathologic reflexes” so narrowly seems to involve attempts to subdivide the “abnormal” reflexes into clinically meaningful subgroups. For example, Massey, Pleet, and Scherokman (1985) specifically define “pathologic reflexes” as “indicators of a pyramidal tract lesion” (p. 64), while labelling some other abnormal reflexes (e.g., sucking, ipsilateral palmomental, and grasp reflexes)—presumably indicative of extensive frontal- lobe damage—as “frontal release signs” (p. 68–71). Some other authors also distinguish a category Called “frontal release signs” or “primitive reflexes” (see D: Primitive reflexes for an ambiguity related to that term), but the particular reflexes listed vary somewhat among texts (compare, for example, DeJ, p. 486–487, to MP&s p. 70–71). Other categories of abnormal reflexes may also be found, such as the “reflexes of spinal automatism” (= “defense reflexes”) described by DeJong (1979, p.464–467).
Frontotemporal Dementia
Published in Marc E. Agronin, Alzheimer's Disease and Other Dementias, 2014
A neurological examination conducted early in the course of FTD may be entirely normal. As the disease progresses, extrapyramidal symptoms (EPS), including bradykinesia and rigidity, commonly emerge, depending on the degree of subcortical involvement and the clinical overlap with corticobasal degeneration, described later in the chapter. Important neurological symptoms that may emerge late in the disease course are as follows: (1) perseveration of both verbal and motor responses, including echolalia (repeating or parroting other individual's words) and echopraxia (mimicking movements) and (2) primitive reflexes that result from upper motor neuron damage to the frontal lobes and corticobulbar tracts, as seen in pseudobulbar palsy (involuntary, paroxysmal episodes of emotion such as laughter or crying). These abnormal reflexes in adults are referred to as frontal release signs, and they include the snout or pouting reflex, the grasp reflex, the sucking reflex, the jaw-jerk reflex, the palmomental (palm-chin) reflex, and the Babinski sign (or extensor plantar reflex).
A case of progressive non-fluent aphasia as onset of amyotrophic lateral sclerosis with frontotemporal dementia
Published in International Journal of Neuroscience, 2019
F. De Marchi, G. Tondo, M.F. Sarnelli, L. Corrado, V. Solara, S. D’Alfonso, R. Cantello, L. Mazzini
In December 2016 bulbar deficits appeared, with dysphagia and dyspnoea for minimal efforts. The neurological examination showed: dysarthria, dysphagia, normal tongue without fasciculations, neck weakness; mild hypotrophy and concomitant distal weakness of the upper and lower limbs, with fasciculations at the lower limbs; diffusely brisk tendon reflexes, with mute plantar response; frontal release signs. The needle electromyography showed a lower-motor-neuron involvement and fasciculations in bulbar, cervical and lumbar districts. According to El Escorial Criteria [13], in January 2017, a diagnosis of definite sporadic ALS with bulbar onset was made. The clinical picture rapidly worsened: the patients underwent a Percutaneous Endoscopic Gastrostomy and he started Non Invasive Ventilation in February 2017. He died in February 2018 for respiratory failure.
Alcohol addiction - the safety of available approved treatment options
Published in Expert Opinion on Drug Safety, 2018
Mariangela Antonelli, Anna Ferrulli, Luisa Sestito, Gabriele A. Vassallo, Claudia Tarli, Carolina Mosoni, Maria M. Rando, Antonio Mirijello, Antonio Gasbarrini, Giovanni Addolorato
Neurological adverse events account for 28% of all disulfiram side effects, making the nervous system the most affected apparatus by disulfiram toxicity [82]. Disulfiram neurotoxicity is mostly attributable to the accumulation of acetaldehyde and other toxic metabolites, such as carbon disulfide. This mechanism is mainly involved in the development of polyneuropathy which causes ataxia, paresthesias, and optic neuritis [83]. It seems to be dose-dependent and independent from gender and age [84]. In addition, other disulfiram neurotoxic side effects are attributable to the inhibition of dopamine-β-hydroxylase, an enzyme that catalyzes the conversion of dopamine to noradrenaline, affecting the level of brain biogenic amines [85]. Headache, delirium, convulsions, myoclonus, dysarthria, frontal release signs, anxiety, impaired memory, decreased concentration, depression, and psychosis could be related to this pathophysiological mechanism [86]. Moreover, the use of disulfiram in alcohol dependent patients may worsen preexisting conditions, such as alcoholic polyneuropathy and Wernicke encephalopathy [87].
HD-tDCS as a neurorehabilitation technique for a case of post-anoxic leukoencephalopathy
Published in Neuropsychological Rehabilitation, 2022
Sarah Garcia, Benjamin M. Hampstead
Given the widespread injury that occurs with PAL, it is unsurprising that cognitive deficits have been reported in virtually all domains including attention, language, executive function, and learning and memory (Anderson & Arciniegas, 2010; Shprecher & Mehta, 2010; Victor & Ropper, 2001). Associated personality and behavioural changes can be wide-ranging but often include emotional lability, impulsivity, and irritability (Anderson & Arciniegas, 2010). In more severe cases, PAL can also lead to frontal release signs and symptoms typically seen in psychosis (Shprecher & Mehta, 2010).