Skip to main content
Brain and Behavior logoLink to Brain and Behavior
. 2024 Nov 22;14(11):e70164. doi: 10.1002/brb3.70164

Detailed Analysis of the Palmomental Reflex and Its Clinical Significance

Benxu Ma 1, Jianying Zhang 2, Yanlei Cui 2, Huanmin Gao 2,
PMCID: PMC11583821  PMID: 39576271

ABSTRACT

Purpose

This comprehensive review thoroughly explores the clinical significance of the palmomental reflex (PMR) in neurological disorders. PMR is a primitive reflex that, when reemerging in adults, indicates underlying neurological dysfunction.

Method

The article elaborates on the clinical assessment techniques, neurophysiological basis, and applications of PMR in various neurological disorders, including neurodegenerative diseases, cerebrovascular disorders, traumatic brain injury, and multiple sclerosis.

Finding

By understanding the modulation and suppression mechanisms of PMR, valuable insights into the specific neurological impairments associated with these disorders can be gained.

Conclusion

The potential of PMR as a diagnostic marker, prognostic indicator, and treatment monitoring tool is increasingly evident.

Keywords: clinical significance, neurological disorders, palmomental reflex (PMR)


The palmomental reflex, a primitive reflex typically absent in adults, reemerges in various neurological disorders. Its presence and characteristics offer valuable insights for diagnosis, disease progression assessment, and treatment monitoring across conditions such as Parkinson's disease, Alzheimer's disease, stroke, and traumatic brain injury.

graphic file with name BRB3-14-e70164-g001.jpg

1. Introduction

The human nervous system is characterized by the presence of various primitive reflexes, which are typically observed in infancy but tend to diminish or disappear as the brain matures and inhibitory mechanisms develop (Touwen 1995). However, in certain neurological conditions, these primitive reflexes may reemerge, providing valuable clinical insights into underlying neurological dysfunction (Paulson and Gottlieb 1968). Among these reflexes, the palmomental reflex (PMR) has garnered significant attention due to its potential diagnostic and prognostic implications across a wide range of neurological disorders (Choi et al. 2011).

PMR, also known as the Marinescu–Radovici reflex or the Mendel–Bechterew reflex, refers to the involuntary contraction of the mentalis muscle (the muscle protruding the chin) in response to a firm, sustained stroke or scratch on the thenar eminence (the fleshy base of the thumb; Owen and Mulley 2002). This reflex is considered a pathological sign in adulthood, as it typically disappears after the first few years of life, when cortical inhibitory mechanisms become well‐established (Zafeiriou 2004).

The reemergence of PMR in adults is often associated with disruptions or dysfunctions in the neural pathways responsible for the inhibition and modulation of this primitive reflex (Reis 1961). Consequently, the presence of PMR may serve as an indicator of underlying neurological impairments, making it a potentially valuable diagnostic tool in various neurological conditions (Marterer‐Travniczek et al. 1992).

1.1. Historical Background

PMR was first described independently by several researchers in the late 19th and early 20th centuries, including Marinescu, Radovici, Mendel, and Bechterew (Dalby 1970). These pioneers observed the reflex response in infants and noted its subsequent disappearance during normal development (Gabelle et al. 2016). However, they also recognized the reappearance of PMR in certain neurological disorders, prompting further investigation into its clinical significance (Little and Masotti 1974).

Since its initial discovery, PMR has been extensively studied and documented in various neurological conditions, ranging from neurodegenerative diseases to stroke, traumatic brain injury (TBI), and multiple sclerosis (MS) (Vreeling 1994). Numerous research efforts have been dedicated to understanding the neuroanatomical and neurophysiological underpinnings of PMR, as well as its potential utility as a diagnostic and prognostic marker (Van Gijn 1977).

1.2. Clinical Relevance and Significance

The clinical relevance of PMR lies in its potential to provide insights into the functional integrity of specific neural pathways and brain regions involved in the inhibition and modulation of primitive reflexes (Brodal 1981). The presence of PMR in adulthood may indicate disruptions or dysfunction in frontal lobe regions, corticobulbar tracts, extrapyramidal systems, or cortical inhibitory mechanisms, all of which play crucial roles in the suppression of this reflex (Walterfang and Velakoulis 2005).

By assessing the presence and characteristics of PMR, clinicians can potentially gain valuable information about the underlying neurological impairments and the extent of neurological involvement in various disorders (Gossman and Jacobs 1980). Additionally, PMR may serve as a prognostic indicator, providing insights into disease progression, treatment response, and overall clinical outcomes in certain neurological conditions (Polunina 2011).

This comprehensive review aims to provide a comprehensive overview of PMR, including its clinical assessment, neurophysiological basis, and implications in various neurological disorders. By synthesizing the latest research findings and clinical perspectives, this review seeks to enhance the understanding and utility of PMR as a valuable diagnostic and prognostic tool in the field of neurology (Okuda et al. 2008).

2. Clinical Assessment of the Palmomental Reflex

The accurate and consistent assessment of PMR is crucial for its effective utilization as a diagnostic and prognostic marker in neurological disorders. This section outlines standardized techniques for eliciting and evaluating PMR, addressing potential confounding factors, and strategies for enhancing the accuracy of the assessment.

2.1. Elicitation Techniques

PMR is typically elicited by delivering a firm, sustained stroke or scratch to the thenar eminence (the fleshy base of the thumb) using a blunt object, such as the handle of a reflex hammer or a key (Lupescu et al. 2020). The stimulation should be applied with sufficient pressure to evoke a response while avoiding excessive discomfort or pain for the patient (Vidovic et al. 2021). Researchers have proposed various specific techniques for eliciting PMR, each with its unique advantages and considerations. Some of the commonly employed methods include:

  1. Stroking technique: The examiner firmly strokes the thenar eminence in a unidirectional manner, applying consistent pressure and maintaining a steady pace (Wallace et al. 2021). The stroke should be sustained for several seconds, typically ranging from 5 to 10 s, to allow sufficient time for the reflex response to manifest (Melillo et al. 2023).

  2. Scratching technique: An alternative approach involves scratching the thenar eminence with a blunt object, such as a key or the end of a reflex hammer (Abraham, Reinhart, and Svoboda 2002). The scratching motion should be firm and sustained, covering a small area of the thenar eminence for several seconds (Lenggenhager 2009).

  3. Repetitive tapping technique: This technique involves delivering a series of firm taps or percussions with a blunt object to the thenar eminence, maintaining a consistent rhythm and pressure (Zanoni et al. 2023; Whittle and Miller 1987).

While these techniques have been widely employed, there is currently no consensus on the optimal method for eliciting PMR. The choice of technique may depend on factors such as examiner preference, patient comfort, and the specific clinical context (Oli and Shrestha 2024). Regardless of the technique used, it is essential to ensure consistency and standardization within and across clinical settings to facilitate accurate comparisons and interpretation of the reflex response.

2.2. Assessing the Reflex Response

The evaluation of PMR involves carefully observing and grading the contraction of the mentalis muscle, which is responsible for protruding the chin (Niedermeyer 1998). A positive PMR is characterized by a visible contraction or twitching of the mentalis muscle in response to the stimulation of the thenar eminence (Walther et al. 2013).

It is important to note that the reflex response may vary in intensity and duration, ranging from a brief, subtle contraction to a sustained, forceful contraction of the mentalis muscle (Gieysztor, Choińska, and Paprocka‐Borowicz 2018). The assessment of PMR should take into account both the presence and the characteristics of the reflex response, as these factors may provide valuable insights into the underlying neurological condition (Tankisi et al. 2021).

Several key aspects should be considered when assessing PMR. The examiner should note the time elapsed between the stimulation and the onset of the reflex response, as well as the duration of the contraction (Modrell and Tadi 2023). A prompt onset and prolonged duration of the reflex may suggest more severe neurological involvement (Pecuch et al. 2021). The intensity and strength of the mentalis muscle contraction should be evaluated, ranging from mild to pronounced or forceful contractions (Goyal et al. 2022). More intense contractions may be associated with greater neurological dysfunction or disinhibition of the reflex (Gramespacher et al. 2020). In some cases, the reflex response may extend beyond the mentalis muscle, involving other perioral or facial muscles, such as the orbicularis oris (muscles around the mouth) or the platysma (neck muscle) (Byers and Dodge 1967). The spread or radiation of the reflex to adjacent muscles should be documented, as it may provide additional insights into the extent of neurological involvement (Yadav, Mahale, and Pal 2018). The examiner should assess whether the reflex response is unilateral (occurring on one side of the face) or bilateral (occurring on both sides) (André 2023). Asymmetrical or unilateral responses may suggest localized or lateralized neurological dysfunction (Camarda et al. 2019). For example, a stronger PMR on the right side of the chin in response to stimulation of the right hand may indicate dysfunction in the left hemisphere of the brain.

To standardize the assessment and facilitate consistent comparisons, various grading systems have been proposed for evaluating the intensity and characteristics of PMR (Cattaneo and Pavesi 2014). One widely adopted grading system categorizes PMR into four levels based on the duration and strength of the reflex response (Tsuyusaki et al. 2016): Absent (no visible contraction of the mentalis muscle upon stimulation); Present (mild contraction of the mentalis muscle, lasting less than 5 s); Brisk (moderate‐to‐strong contraction of the mentalis muscle, lasting 5–10 s); and Persistent (sustained contraction of the mentalis muscle, lasting more than 10 s). By adhering to standardized grading systems and documenting the specific characteristics of the reflex response, clinicians can enhance the objectivity and reproducibility of PMR assessment, enabling more accurate comparisons and monitoring over time (de Noordhout and Delwaide 1988).

2.3. Addressing False Negatives and Confounding Factors

While the presence of PMR is generally considered a pathological sign in adulthood, the absence of the reflex does not necessarily indicate a lack of neurological impairment (Borg, Warwick, and Ahmed 2021). Various factors can potentially contribute to false‐negative results, where PMR is not elicited despite underlying neurological dysfunction (Dickson 1998). Recognizing and addressing these confounding factors is crucial for enhancing the accuracy and reliability of PMR assessment.

2.3.1. Cognitive Impairment

Patients with significant cognitive impairment or decreased levels of consciousness may not exhibit PMR, even in the presence of neurological dysfunction (Ghosh Md et al. 2022). In such cases, the ability to follow instructions and maintain attention during the examination can be compromised, potentially leading to false‐negative results (Camarda et al. 2020).

2.3.2. Muscular Weakness or Paresis

Neuromuscular disorders or other conditions resulting in significant muscular weakness or paresis may hinder the visible manifestation of PMR (Peddireddy et al. 2006). If the mentalis muscle or associated facial muscles are severely weakened, the reflex contraction may not be apparent, despite the underlying neurological impairment (Noda et al. 2015).

2.3.3. Peripheral Neuropathy

In cases of severe peripheral neuropathy or damage to the sensory nerves supplying the thenar eminence, the afferent pathway necessary for eliciting PMR may be disrupted, leading to an absent reflex response (Klein et al. 1997).

2.3.4. Examiner Experience and Technique

The experience and technique of the examiner play a crucial role in the accurate assessment of PMR (Burrell et al. 2016). Inexperienced examiners or those who do not employ proper stimulation techniques may fail to elicit the reflex, resulting in false‐negative findings (Clark et al. 1998). If the initial assessment yields a negative result, it is recommended to repeat the examination multiple times, varying the stimulation technique or applying stronger stimuli (Matuszkiewicz and Gałkowski 2021); to encourage the patient to remain attentive and engaged during the examination (Swapna et al. 2020); to evaluate the strength and function of the facial muscles, particularly the mentalis muscle; and to rule out muscular weakness as a contributing factor (De Renzi, Pieczuro, and Vignolo 1966). In cases of suspected peripheral neuropathy or sensory deficits, additional tests, such as electrophysiological studies or sensory examinations, may be warranted to assess the integrity of the afferent pathway (Lusins and Bender 1973). Moreover, examiners should be ensured to receive proper training and adhere to standardized protocols for eliciting and assessing PMR, minimizing variability and enhancing consistency (Khan et al. 2021). By recognizing and addressing these confounding factors and implementing appropriate strategies, clinicians can enhance the diagnostic accuracy and reliability of PMR assessment, ultimately contributing to more informed clinical decision‐making (Isakov et al. 1984).

3. Neurophysiological Basis of the Palmomental Reflex

Understanding the neurophysiological mechanisms underlying PMR is crucial for interpreting its clinical significance and implications in various neurological disorders. This section explores the neural pathways, brain regions, and neurotransmitter systems involved in the modulation and suppression of PMR, shedding light on the potential neurological underpinnings of its reemergence in adulthood.

3.1. Neural Pathways and Brain Regions

PMR is a complex reflex involving multiple neural pathways and brain regions responsible for its elicitation, modulation, and suppression (Dutta et al. 2016). The afferent pathway for PMR originates from the sensory neurons innervating the thenar eminence, specifically the palmar branch of the median nerve (Rosenbohm et al. 2014). These sensory fibers convey tactile information from the stimulated area to the spinal cord and subsequently to higher brain regions for processing and integration (Thompson and Thompson 2023). At the level of the spinal cord and brainstem, the afferent signals from the thenar eminence are relayed through various interneuronal connections and ascending pathways (Swash et al. 2020). The reticular formation, a network of nuclei within the brainstem, is thought to play a crucial role in modulating and integrating PMR response (Iwasaki 2006).

The frontal lobe, particularly the prefrontal cortex and supplementary motor areas, is believed to be a key region involved in the inhibition and modulation of PMR (Spreen and Risser 2003). These areas exert their influence on the reflex through descending corticobulbar pathways, which connect the frontal lobe to the brainstem and spinal cord (Alves et al. 2009). The basal ganglia, a group of subcortical nuclei, and the associated extrapyramidal system are also implicated in the modulation of PMR (Nicholson and Pereira 2002). Structures such as the caudate nucleus, putamen, and globus pallidus are thought to play a role in the inhibition and regulation of primitive reflexes, including PMR (Bala et al. 2023). However, the exact neural circuitry is not fully elucidated yet.

Various neurotransmitter systems are involved in the modulation and suppression of PMR, including dopaminergic, cholinergic, and GABAergic pathways (Vreeling et al. 1994). Disruptions or imbalances in these neurotransmitter systems may contribute to the disinhibition and reemergence of PMR in certain neurological conditions (Caccia et al. 1996).

While the precise neuroanatomical and neurochemical mechanisms underlying PMR are still under investigation, it is clear that this reflex involves a complex interplay of neural pathways, brain regions, and neurotransmitter systems (Barabas and Matthews 1997). The reemergence of PMR in adulthood may reflect disruptions or dysfunctions in any of these components, providing insights into the underlying neurological impairments (Shahed and Jankovic 2007).

3.2. Developmental Aspects and Inhibitory Mechanisms

PMR is one of several primitive reflexes that can be used to diagnose neurological disorders. Other primitive reflexes, such as the snout reflex and jaw reflex, may also be present in certain neurological conditions. However, PMR has been shown to be a particularly useful diagnostic tool in certain contexts, such as in the diagnosis of Parkinson's disease (PD).

The disappearance of PMR during typical childhood development is attributed to the maturation of cortical inhibitory mechanisms and the establishment of higher order control over primitive reflexes (Shargorodsky, Lin, and Gopen 2010). As the brain develops, the prefrontal cortex and associated neural networks responsible for inhibitory control become more efficient, effectively suppressing the expression of primitive reflexes like PMR (Prajjwal et al. 2023).Primitive reflexes such as the snout, jaw, and grasp reflexes may also provide insights into neurological dysfunction.

The reemergence of PMR in adulthood is often considered a manifestation of disinhibition or a release of these primitive reflexes from cortical control (Moura et al. 2023). This disinhibition may result from various neurological insults or degenerative processes that disrupt the inhibitory mechanisms or the neural pathways involved in the modulation of PMR (Camarda et al. 2018).

By understanding the developmental aspects and inhibitory mechanisms underlying PMR, researchers and clinicians can gain insights into the neurodevelopmental and neurodegenerative processes that may contribute to the reemergence of this reflex in various neurological disorders (Güney et al. 2023).

4. Palmomental Reflex in Neurological Disorders

PMR has been extensively studied and documented in a wide range of neurological disorders, providing valuable diagnostic and prognostic information. This section explores the clinical implications and significance of PMR in various neurological conditions, highlighting its potential utility as a marker of disease progression and treatment response. The characteristic features of PMR may vary across different neurological disorders. For example, the intensity and duration of PMR may be more pronounced in patients with PD compared to those with Alzheimer's disease (AD) (Aguilar Agudo, Herruzo Cabrera, and Pino Osuna 2021).

4.1. Parkinson's Disease

In PD, the presence of PMR has been consistently observed and is considered a common clinical finding (Mandelbaum and Marks 2020). The reemergence of PMR in PD is thought to be related to the degeneration of dopaminergic neurons in the substantia nigra and the subsequent disruption of frontal–subcortical circuits involved in the inhibition of primitive reflexes (Sanchez‐Ramos, Ortoll, and Paulson 1996).

The presence and severity of PMR in PD patients have been associated with disease progression, cognitive impairment, and the development of levodopa‐induced dyskinesias (Wibawa et al. 2023). Additionally, PMR has been proposed as a potential marker for the early detection of PD, as it may precede the onset of cardinal motor symptoms in some cases (Cruccu et al. 2005).

Recent studies have also explored the relationship between PMR and specific PD subtypes or phenotypes, suggesting that the presence and characteristics of the reflex may vary depending on the underlying neuropathological patterns (Sigafoos et al. 2021). By monitoring the evolution of PMR, clinicians gain valuable insights into disease progression and treatment response, enabling more informed clinical decision‐making.

4.2. Alzheimer's Disease and Other Dementias

PMR has been observed in patients with AD and other forms of dementia, potentially reflecting the cognitive and neurological changes associated with these neurodegenerative conditions (Burns, Jacoby, and Levy 1991). In AD, the presence of PMR is thought to be related to the degeneration of frontal lobe structures and the disruption of cortical inhibitory mechanisms responsible for suppressing primitive reflexes (Sabayan et al. 2012).

Studies have suggested that PMR may be more prevalent in the later stages of AD, when cognitive impairment and frontal lobe dysfunction are more pronounced (Karpenko and Keegan 2021). Additionally, the presence and severity of PMR have been correlated with the degree of cognitive impairment and functional decline in AD patients (Chiang et al. 2005).

In vascular dementia and other forms of dementia, PMR may arise from the disruption of frontal–subcortical circuits or the presence of subcortical lesions affecting the pathways involved in reflex modulation (Coebergh and Stanton 2020). The assessment of PMR can provide valuable insights into the underlying neuropathological processes and the extent of neurological involvement in these dementia subtypes.

4.3. Multiple System Atrophy

PMR has also been documented in other neurodegenerative disorders, such as multiple system atrophy (MSA) (Thomas 1994). In MSA, PMR has been associated with the degeneration of extrapyramidal and cerebellar systems (Novak and Tabrizi 2011; Melillo et al. 2022). By assessing the presence and characteristics of PMR in these neurodegenerative disorders, clinicians can gain insights into the underlying neuropathological processes and potentially differentiate between various subtypes or phenotypes (Frank, Pari, and Rossiter 2006).

4.4. Stroke

PMR is frequently observed in patients who have suffered from stroke, particularly in cases involving lesions or dysfunction in the frontal lobe, basal ganglia, or corticobulbar pathways (Schott and Rossor 2016). The presence of PMR in stroke patients has been associated with the location and extent of the lesion, as well as the severity of neurological impairment (Morningstar et al. 2005).

In ischemic stroke, PMR may be observed in the acute phase or may develop over time as a result of reorganization and neuroplasticity processes (Zhang et al. 2021). The appearance of PMR in these cases may reflect the disruption of inhibitory mechanisms or the disinhibition of primitive reflexes due to the lesion or dysfunction in specific brain regions (Damasceno et al. 2005).

In hemorrhagic stroke, the presence of PMR has been linked to the location and extent of the hematoma, particularly when involving subcortical or frontal lobe regions (Rao, Jackson, and Howard 1999). The assessment of PMR can provide valuable prognostic information and insights into the functional recovery and rehabilitation potential in stroke patients (Dünser et al. 2018).

4.5. Vascular Dementia and Cognitive Impairment

In vascular dementia and other forms of vascular cognitive impairment, PMR has been observed and may be related to the presence of subcortical lesions, white matter changes, or disruptions in frontal–subcortical circuits (Coebergh and Stanton 2020). The assessment of PMR can aid in the differential diagnosis of vascular cognitive impairment and may provide insights into the underlying neuropathological processes and the extent of neurological involvement.

4.6. Traumatic Brain Injury

PMR is commonly observed in patients who have suffered from TBI, particularly in cases involving frontal lobe damage or diffuse axonal injury (Martello 2023). The presence of PMR in TBI patients has been associated with the severity of the injury, cognitive impairment, and the development of chronic neurological deficits (Miles et al. 2021).

In mild TBI or concussion, PMR may be a transient finding, potentially reflecting a temporary disruption of inhibitory mechanisms or a functional diaschisis (Wijdicks 2021). However, in cases of moderate‐to‐severe TBI, the persistent presence of PMR may indicate more extensive structural damage or neuronal loss, particularly in frontal lobe regions or corticobulbar pathways (Jose, Samuel, and Isabel 2020).

The assessment of PMR can provide valuable information for the prognosis and rehabilitation planning of TBI patients, as the presence and characteristics of the reflex may be indicative of the extent of neurological impairment and the potential for functional recovery (Sucksdorff et al. 2020).

4.7. Multiple Sclerosis

In patients with MS, PMR has been observed and may be related to the presence of demyelinating lesions or plaques affecting the neural pathways involved in the modulation of primitive reflexes (Gramespacher et al. 2020). PMR may be more prevalent in specific subtypes of MS, such as primary progressive MS or secondary progressive MS, where cortical and subcortical pathways are more extensively affected (Ragab et al. 2021).

The presence and characteristics of PMR in MS patients have been associated with disease progression, cognitive impairment, and the development of physical disabilities (Mantel et al. 2017). The assessment of PMR can provide valuable insights into the extent of neurological involvement and the potential impact on functional abilities in MS patients.

4.8. Other Neurological Conditions

PMR has been documented in various other neurological conditions, including brain tumors (Ho et al. 2013), epilepsy (Konicarova, Bob, and Raboch 2013), neurodevelopmental disorders (Bonti et al. 2024), metabolic and toxic encephalopathies (Xu et al. 2024). In these diverse neurological conditions, the presence and characteristics of PMR can provide valuable diagnostic and prognostic information, contributing to a better understanding of the underlying neurological impairments and potential treatment strategies (Zafeiriou, Tsikoulas, and Kremenopoulos 1995).

5. Clinical Implications and Future Directions

The assessment of PMR holds significant clinical utility and implications across various neurological disorders. This section discusses the potential applications of PMR in diagnosis, prognosis, and treatment monitoring, as well as the challenges and limitations that should be addressed in future research endeavors.

5.1. Diagnostic Applications

The presence of PMR in adulthood is generally considered a pathological sign, indicating the presence of underlying neurological dysfunction (di Biase et al. 2022). While PMR is not specific to any particular neurological disorder, its assessment can provide valuable diagnostic information when interpreted in the context of other clinical findings and neurological examinations.

In clinical practice, PMR can serve as a screening tool or an adjunctive diagnostic marker, prompting further investigations or neuroimaging studies to identify the underlying cause (Mattson 2023). For example, the presence of PMR in a patient with cognitive impairment or motor symptoms may support the diagnosis of a neurodegenerative disorder or cerebrovascular disease, and guide the selection of appropriate diagnostic tests (Harwood and Cowan 2020).

Additionally, the specific characteristics of PMR, such as its intensity, duration, and laterality, may provide insights into the localization or extent of the neurological impairment, aiding in the differential diagnosis and targeted evaluation (Faglioni 2020).

5.2. Prognostic Implications

Beyond its diagnostic value, PMR has shown promise as a potential prognostic marker in various neurological disorders. The presence, severity, and evolution of PMR over time can provide insights into disease progression, functional outcomes, and treatment response.

In neurodegenerative diseases, such as PD and AD, the presence and severity of PMR have been associated with cognitive decline, functional impairment, and the development of complications (Vallar 2020). Regular monitoring of PMR may help clinicians track disease progression and inform treatment decisions or adjustments (Harp et al. 2022).

In stroke and TBI, PMR can serve as a prognostic indicator of functional recovery and rehabilitation potential (Asadi et al. 2021). The persistence or resolution of PMR over time may reflect the extent of neuroplasticity and neural reorganization, guiding therapeutic interventions.

5.3. Treatment Monitoring and Response Evaluation

The assessment of PMR can also play a role in monitoring treatment response and evaluating the effectiveness of therapeutic interventions in various neurological disorders. By tracking changes in the presence, intensity, or characteristics of PMR, clinicians can gain insights into the impact of pharmacological or nonpharmacological treatments on the underlying neural pathways and inhibitory mechanisms.

In PD, for instance, the resolution or attenuation of PMR following dopaminergic treatment or deep brain stimulation may indicate a positive response and improved modulation of primitive reflexes (Drenth et al. 2020). Conversely, the persistence or exacerbation of PMR despite treatment may suggest the need for treatment adjustments or the exploration of alternative therapeutic approaches.

Similarly, in MS, PMR can be used as a marker to evaluate the efficacy of disease‐modifying therapies or rehabilitation interventions (Lochhead et al. 2020). Changes in PMR over time may reflect the extent of remyelination, neuroplasticity, or functional recovery, guiding treatment decisions and rehabilitation strategies.

5.4. Challenges and Limitations

PMR holds significant potential as a diagnostic and prognostic tool (Table 1). Despite the availability of various elicitation and grading methods, there is a lack of consensus on standardized protocols for assessing PMR (Alnajashi and Alyazidi 2023). Establishing universally accepted guidelines and protocols can improve the consistency and comparability of findings across different clinical settings and research studies. Efforts should be made to improve inter‐rater reliability through comprehensive training programs and the use of objective measurement techniques, such as electromyography or motion capture systems (Jankovic and Lang 2021). As PMR is a nonspecific sign, its diagnostic value may be limited in certain clinical scenarios (Ticku et al. 2022). Further research is needed to establish the specificity and sensitivity of PMR in various neurological disorders, as well as its ability to differentiate between different pathological conditions.

TABLE 1.

Summary of PMR in neurological disorders.

Neurological disorder Prevalence of PMR Diagnostic ability Prognostic ability References
Parkinson's disease Common clinical finding Potential early detection marker; may precede cardinal motor symptoms Associated with disease progression, cognitive impairment, and levodopa‐induced dyskinesias Mandelbaum and Marks (2020), Sanchez‐Ramos, Ortoll, and Paulson (1996), Wibawa et al. (2023), and Cruccu et al. (2005)
Alzheimer's disease More prevalent in later stages Reflects cognitive and neurological changes; correlated with degree of cognitive impairment Associated with functional decline Burns, Jacoby, and Levy (1991), Sabayan et al. (2012), Karpenko and Keegan (2021), and Chiang et al. (2005)
Multiple system atrophy Documented presence Associated with degeneration of extrapyramidal and cerebellar systems May aid in differentiating subtypes or phenotypes Thomas (1994), Novak and Tabrizi (2011), Melillo et al. (2022), and Frank, Pari, and Rossiter (2006)
Stroke Frequent observation, particularly with frontal lobe, basal ganglia, or corticobulbar pathway involvement Associated with lesion location and extent; reflects neurological impairment severity Provides insights into functional recovery and rehabilitation potential Schott and Rossor (2016), Morningstar et al. (2005), Zhang et al. (2021), Damasceno et al. (2005), Rao, Jackson, and Howard (1999), and Dünser et al. (2018)
Vascular dementia Observed presence Related to subcortical lesions and white matter changes May aid in differential diagnosis Coebergh and Stanton (2020)
Traumatic brain injury Common, especially with frontal lobe damage Associated with injury severity and cognitive impairment Indicator of chronic neurological deficits; useful for rehabilitation planning Martello (2023), Miles et al. (2021), Wijdicks (2021), Jose, Samuel, and Isabel (2020), and Sucksdorff et al. (2020)
Multiple sclerosis Observed presence, more prevalent in progressive subtypes Related to demyelinating lesions affecting neural pathways Associated with disease progression, cognitive impairment, and physical disabilities Gramespacher et al. (2020), Ragab et al. (2021), and Mantel et al. (2017)

While PMR can provide valuable insights, it should be interpreted in conjunction with other clinical findings, neuroimaging data, and laboratory investigations (León‐Bravo, Cantarero‐Carmona, and Caballero‐Villarraso 2023). For example, when evaluating a patient with suspected PD, clinicians may consider the presence of other motor symptoms, such as tremors, rigidity, and bradykinesia, in addition to PMR. Similarly, in patients with suspected stroke, clinicians may consider the results of neuroimaging studies, such as CT or MRI scans, in conjunction with PMR. Developing integrative approaches that combine PMR with other diagnostic and prognostic markers can enhance the accuracy and reliability of clinical decision‐making. In addition, longitudinal studies involving repeated assessments of PMR in various neurological disorders are needed to fully elucidate its utility as a prognostic and monitoring tool (Lundblad et al. 2020).

By addressing these challenges and limitations through collaborative efforts among researchers, clinicians, and healthcare professionals, the clinical utility and reliability of PMR assessment can be enhanced, ultimately contributing to improved diagnostic accuracy, prognostic evaluation, and treatment monitoring in various neurological disorders.

6. Conclusion

PMR has emerged as a valuable clinical tool in the field of neurology, offering insights into the functional integrity of neural pathways and inhibitory mechanisms involved in the modulation of primitive reflexes in adulthood, to indicate an underlying neurological dysfunction. Through this comprehensive review, we have explored the clinical assessment techniques, neurophysiological basis, and diverse applications of PMR across a wide range of neurological disorders. From neurodegenerative diseases and cerebrovascular disorders to TBI and MS, PMR has demonstrated its potential as a diagnostic marker, prognostic indicator, and treatment monitoring tool.

By understanding the neural pathways, brain regions, and neurotransmitter systems involved in the modulation and suppression of PMR, researchers and clinicians can gain valuable insights into the specific neurological impairments associated with its reemergence in various conditions. In addition, the developmental aspects and inhibitory mechanisms underlying PMR provide a window into the neurodevelopmental and neurodegenerative processes that contribute to its manifestation.

As this primitive reflex holds the potential to become an increasingly valuable tool in the diagnostic armamentarium of clinicians. By leveraging the insights gained from PMR, we can potentially improve patient care, refine treatment strategies, and advance our understanding of the intricate workings of the human nervous system.

Author Contributions

Benxu Ma: conceptualization, methodology, writing–original draft, writing–review and editing. Jianying Zhang: conceptualization, methodology, writing–original draft, writing–review and editing. Yanlei Cui: formal analysis, writing–original draft, writing–review and editing. Huanmin Gao: writing–original draft, writing–review and editing.

Consent

The authors have nothing to report.

Conflicts of Interest

The authors declare no conflicts of interest.

Peer Review

The peer review history for this article is available at https://publons.com/publon/10.1002/brb3.70164.

Acknowledgments

The authors have nothing to report.

Funding: The authors received no specific funding for this work.

Benxu Ma and Jianying Zhang contributed equally to this work.

Data Availability Statement

All data generated or analyzed during this study are included in this published article.

References

  1. Abraham, E. , Reinhart K., and Svoboda P.. 2002. “Sepsis.” Intensive Care 137: 789–793. [Google Scholar]
  2. Aguilar Agudo, A. , Herruzo Cabrera J., and Pino Osuna M. J.. 2021. “Effects of Progressive Muscle Relaxation on Levodopa‐Induced Dyskinesia.” Psychology and Neuroscience 14, no. 2: 218–225. [Google Scholar]
  3. Alnajashi, H. A. , and Alyazidi A. S.. 2023. “The Important Role of Family Members in Guiding Medical Professions to Reach a Diagnosis: Case Report of Under‐Noticed Bilateral Apraxia of Eyelid Closure.” Journal of Family Medicine and Primary Care 12, no. 6: 1222–1225. [DOI] [PMC free article] [PubMed] [Google Scholar]
  4. Alves, G. , Müller B., Herlofson K., et al. 2009. “Incidence of Parkinson's Disease in Norway: The Norwegian ParkWest Study.” Journal of Neurology, Neurosurgery and Psychiatry 80, no. 8: 851–857. [DOI] [PubMed] [Google Scholar]
  5. André, C. 2023. “Alf Brodal's Stroke in 1972: A Brilliant Self‐Report by a Neuroanatomy Professor.” Revue Neurologique 179, no. 4: 251–255. [DOI] [PubMed] [Google Scholar]
  6. Asadi, S. , Ghadirivasfi M., Alavi K., et al. 2021. “Clinical Features of Patients Newly Admitted to the Emergency Department of a Psychiatric Hospital With an Emphasis on Physical Examination.” Frontiers in Emergency Medicine 5, no. 1: e4. [Google Scholar]
  7. Bala, J. J. , Bala J. D., Pell J. P., et al. 2023. “Association Between 5‐Min Apgar Score and Attention Deficit Hyperactivity Disorder: A Scotland‐Wide Record Linkage Study of 758,423 School Children.” BMC Psychiatry 23, no. 1: 794. [DOI] [PMC free article] [PubMed] [Google Scholar]
  8. Barabas, G. , and Matthews W. S.. 1997. “The Palmo‐Mental Reflex in Cerebral Palsy.” Journal of Developmental and Physical Disabilities 9: 337–346. [Google Scholar]
  9. Bonti, E. , Zerva I. K., Koundourou C., et al. 2024. “The High Rates of Comorbidity Among Neurodevelopmental Disorders: Reconsidering the Clinical Utility of Distinct Diagnostic Categories.” Journal of Personalized Medicine 14, no. 3: 300. [DOI] [PMC free article] [PubMed] [Google Scholar]
  10. Borg, T. M. , Warwick A. S., and Ahmed M.. 2021. “The Child With Facial Nerve Palsy.” InnovAiT 14, no. 12: 742–748. [Google Scholar]
  11. Brodal, A. 1981. Neurological Anatomy in Relation to Clinical Medicine, 3rd ed. New York, NY: Oxford University Press. [Google Scholar]
  12. Burns, A. , Jacoby R., and Levy R.. 1991. “Neurological Signs in Alzheimer's Disease.” Age and Ageing 20, no. 1: 45–51. [DOI] [PubMed] [Google Scholar]
  13. Burrell, J. R. , Halliday G. M., Kril J. J., et al. 2016. “The Frontotemporal Dementia‐Motor Neuron Disease Continuum.” Lancet 388, no. 10047: 919–931. . [DOI] [PubMed] [Google Scholar]
  14. Byers, R. K. , and Dodge J. A.. 1967. “Huntington's Chorea in Children: Report of Four Cases.” Neurology 17, no. 6: 587–587. [DOI] [PubMed] [Google Scholar]
  15. Caccia, M. R. , Galimberti V., Valla P., Osio M., Dezuanni E., and Mangoni A.. 1996. “Electrophysiology of the Palmomental Reflex in Normal and Parkinsonian Subjects.” Electromyography and Clinical Neurophysiology 36, no. 1: 9–13. [PubMed] [Google Scholar]
  16. Camarda, C. , Camarda R., Pipia C., et al. 2020. “Isolated, Subtle Neurological Abnormalities in Mild Cognitive Impairment Types.” Canadian Journal of Neurological Sciences 47, no. 1: 77–91. [DOI] [PubMed] [Google Scholar]
  17. Camarda, C. , Torelli P., Pipia C., et al. 2018. “Association Between Atrophy of the Caudate Nuclei, Global Brain Atrophy, Cerebral Small Vessel Disease and Mild Parkinsonian Signs in Neurologically and Cognitively Healthy Subjects Aged 45–84 Years: A Crosssectional Study.” Current Alzheimer Research 15, no. 11: 1013–1026. [DOI] [PubMed] [Google Scholar]
  18. Camarda, C. , Torelli P., Pipia C., et al. 2019. “Nociceptive Primitive Reflexes in Neurologically and Cognitively Healthy Aging Subjects.” Canadian Journal of Neurological Sciences 46, no. 2: 199–208. [DOI] [PubMed] [Google Scholar]
  19. Cattaneo, L. , and Pavesi G.. 2014. “The Facial Motor System.” Neuroscience and Biobehavioral Reviews 38: 135–159. [DOI] [PubMed] [Google Scholar]
  20. Chiang, H. Y. , Chen C. T., Chien H. F., et al. 2005. “Skin Denervation, Neuropathology, and Neuropathic Pain in a Laser‐Induced Focal Neuropathy.” Neurobiology of Disease 18, no. 1: 40–53. [DOI] [PubMed] [Google Scholar]
  21. Choi, S. M. , Kim B. C., Nam T. S., et al. 2011. “Midbrain Atrophy in Vascular Parkinsonism.” European Neurology 65, no. 5: 296–301. [DOI] [PMC free article] [PubMed] [Google Scholar]
  22. Clark, L. N. , Poorkaj P., Wszolek Z., et al. 1998. “Pathogenic Implications of Mutations in the Tau Gene in Pallido‐Ponto‐Nigral Degeneration and Related Neurodegenerative Disorders Linked to Chromosome 17.” Proceedings of the National Academy of Sciences of the United States of America 95, no. 22: 13103–13107. [DOI] [PMC free article] [PubMed] [Google Scholar]
  23. Coebergh, J. A. , and Stanton B. R.. 2020. “The Neurological Examination in Neuropsychiatry.” In Oxford Textbook of Neuropsychiatry, edited by Agrawal N., Faruqui R., and Bodani M., 23–34. Oxford: Oxford University Press. [Google Scholar]
  24. Cruccu, G. , Iannetti G. D., Marx J. J., et al. 2005. “Brainstem Reflex Circuits Revisited.” Brain 128, no. 2: 386–394. [DOI] [PubMed] [Google Scholar]
  25. Dalby, M. A. 1970. “The Diagnostic Value of the Palmo‐Mental Reflex.” Acta Neurologica Scandinavica 46, no. 4: 601–608. [DOI] [PubMed] [Google Scholar]
  26. Damasceno, A. , Delicio A. M., Mazo D. F. C., et al. 2005. “Primitive Reflexes and Cognitive Function.” Arquivos De Neuro‐Psiquiatria 63: 577–582. [DOI] [PubMed] [Google Scholar]
  27. de Noordhout, A. M. , and Delwaide P. J.. 1988. “The Palmomental Reflex in Parkinson's Disease: Comparisons With Normal Subjects and Clinical Relevance.” Archives of Neurology 45, no. 4: 425–427. [DOI] [PubMed] [Google Scholar]
  28. De Renzi, E. , Pieczuro A., and Vignolo L. A.. 1966. “Oral Apraxia and Aphasia.” Cortex 2, no. 1: 50–73. [Google Scholar]
  29. di Biase, L. , Di Santo A., Caminiti M. L., et al. 2022. “Classification of Dystonia.” Life 12, no. 2: 206. [DOI] [PMC free article] [PubMed] [Google Scholar]
  30. Dickson, D. W. 1998. “Pick's Disease: A Modern Approach.” Brain Pathology 8, no. 2: 339–354. [DOI] [PMC free article] [PubMed] [Google Scholar]
  31. Drenth, H. , Zuidema S., Bautmans I., et al. 2020. “Paratonia in Dementia: A Systematic Review.” Journal of Alzheimer's Disease 78, no. 4: 1615–1637. [DOI] [PMC free article] [PubMed] [Google Scholar]
  32. Dünser, M. W. , Beer R., Petros S., Mer M.. 2018. “The Brain.” In Clinical Examination Skills in the Adult Critically Ill Patient, edited by Dünser M., Dankl D., Petros S., and Mer M., 81–111. Cham: Springer. [Google Scholar]
  33. Dutta, M. , Nath K., Baruah A., et al. 2016. “A Clinical Study of Neurological Soft Signs in Patients With Schizophrenia.” Journal of Neurosciences in Rural Practice 7, no. 03: 393–399. [DOI] [PMC free article] [PubMed] [Google Scholar]
  34. Faglioni, P. 2020. “The Frontal Lobe.” In Handbook of Clinical and Experimental Neuropsychology, edited by Faglioni P., 525–570. London: Psychology Press. [Google Scholar]
  35. Frank, C. , Pari G., and Rossiter J. P.. 2006. “Approach to Diagnosis of Parkinson Disease.” Canadian Family Physician 52, no. 7: 862–868. [PMC free article] [PubMed] [Google Scholar]
  36. Gabelle, A. , Gutierrez L. A., Dartigues J. F., et al. 2016. “Palmomental Reflex a Relevant Sign in Early Alzheimer's Disease Diagnosis?” Journal of Alzheimer's Disease 49, no. 4: 1135–1141. [DOI] [PMC free article] [PubMed] [Google Scholar]
  37. Ghosh Md, R. , Roy D., León‐Ruiz M., Das S., Dubey S., and Benito‐León J.. 2022. “Seropositive Neuromyelitis Optica in a Case of Undiagnosed Ankylosing Spondylitis: A Neuro‐Rheumatological Conundrum.” Qatar Medical Journal 2022, no. 3: 29. [DOI] [PMC free article] [PubMed] [Google Scholar]
  38. Gieysztor, E. Z. , Choińska A. M., and Paprocka‐Borowicz M.. 2018. “Persistence of Primitive Reflexes and Associated Motor Problems in Healthy Preschool Children. Archives of Medical Science.” Archives of Medical Science 14, no. 1: 167–173. [DOI] [PMC free article] [PubMed] [Google Scholar]
  39. Gossman, M. D. , and Jacobs L.. 1980. “Three Primitive Reflexes in Parkinsonism Patients.” Neurology 30, no. 2: 189–192. [DOI] [PubMed] [Google Scholar]
  40. Goyal, S. , Kamble N., Mudabbir M. A. M., et al. 2022. “Determinants of Levodopa Responsiveness in Patients With Vascular Parkinsonism.” Annals of Indian Academy of Neurology 25, no. 6: 1075–1079. [DOI] [PMC free article] [PubMed] [Google Scholar]
  41. Gramespacher, H. , Richter N., Edwin Thanarajah S., et al. 2020. “Aberrant Frontostriatal Connectivity in Alzheimer's Disease With Positive Palmomental Reflex.” European Journal of Neurology 27, no. 12: 2405–2414. [DOI] [PubMed] [Google Scholar]
  42. Güney, G. , Jansen T. S., Braczynski A. K., et al. 2023. “Analyzing the Effect of Age and Gender on the Blink Reflex Using MediaPipe.” Current Directions in Biomedical Engineering 9, no. 1: 423–426. [Google Scholar]
  43. Harp, J. , Koehl L., Van Pelt K., et al. 2022. “Primitive Reflexes and Dementia in Adults With Down Syndrome.” Neurology: Clinical Practice 12, no. 1: 6–13. [DOI] [PMC free article] [PubMed] [Google Scholar]
  44. Harwood, R. H. , and Cowan R.. 2020. “Physical Assessment.” In Oxford Textbook of Old Age Psychiatry, 3rd ed., edited by Dening T., Thomas A., Stewart R., and Taylor J.‐P., 164–182. Oxford: Oxford University Press. [Google Scholar]
  45. Ho, M. L. , Moonis G., Ginat D. T., et al. 2013. “Lesions of the Corpus Callosum.” American Journal of Roentgenology 200, no. 1: W1–W16. [DOI] [PubMed] [Google Scholar]
  46. Isakov, E. , Sazbon L., Costeff H., et al. 1984. “The Diagnostic Value of Three Common Primitive Reflexes.” European Neurology 23, no. 1: 17–21. [DOI] [PubMed] [Google Scholar]
  47. Iwasaki, Y. 2006. “Lack of Hemispheric Localizing Value of the Palmomental Reflex.” Neurology 66, no. 4: 614–614‐a. [DOI] [PubMed] [Google Scholar]
  48. Jankovic, J. , and Lang A. E.. 2021. “Diagnosis and Assessment of Parkinson Disease and Other Movement Disorders.” In Bradley's Neurology in Clinical Practice E‐Book, 310. [Google Scholar]
  49. Jose, R. G. , Samuel A. S., and Isabel M. M.. 2020. “Neuropsychology of Executive Functions in Patients With Focal Lesion in the Prefrontal Cortex: A Systematic Review.” Brain and Cognition 146: 105633. [DOI] [PubMed] [Google Scholar]
  50. Karpenko, A. , and Keegan J.. 2021. “Diagnosis of Coma.” Emergency Medicine Clinics of North America 39, no. 1: 155–172. [DOI] [PubMed] [Google Scholar]
  51. Khan, A. M. , Habib M. A., Hannan M. A., et al. 2021. “Clinical Presentation of Parkinson's Disease: Experience of Using Movement Disorder Society Clinical Diagnostic Criteria for Parkinson's Disease.” Journal of Advances in Medicine and Medical Research 33, no. 16: 183–188. [Google Scholar]
  52. Klein, C. , Kömpf D., Pulkowski U., Moser A., and Vieregge P.. 1997. “A Study of Visual Hallucinations in Patients With Parkinson's Disease.” Journal of Neurology 244, no. 6: 371–377. [DOI] [PubMed] [Google Scholar]
  53. Konicarova, J. , Bob P., and Raboch J.. 2013. “Persisting Primitive Reflexes in Medication‐Naïve Girls With Attention‐Deficit and Hyperactivity Disorder.” Neuropsychiatric Disease and Treatment 9: 1457–1461. [DOI] [PMC free article] [PubMed] [Google Scholar]
  54. Lenggenhager, B. 2009. “Multisensory Processes Underlying Bodily Self‐Consciousness.” PhD diss.
  55. León‐Bravo, G. , Cantarero‐Carmona I., and Caballero‐Villarraso J.. 2023. “Prevalence of Active Primitive Reflexes and Craniosacral Blocks in Apparently Healthy Children and Relationships With Neurodevelopment Disturbances.” Children 10, no. 6: 1014. [DOI] [PMC free article] [PubMed] [Google Scholar]
  56. Little, T. M. , and Masotti R. E.. 1974. “The Palmo‐Mental Reflex in Normal and Mentally Retarded Subjects.” Developmental Medicine and Child Neurology 16, no. 1: 59–63. [DOI] [PubMed] [Google Scholar]
  57. Lochhead, J. J. , Yang J., Ronaldson P. T., et al. 2020. “Structure, Function, and Regulation of the Blood–Brain Barrier Tight Junction in central Nervous System Disorders.” Frontiers in Physiology 11: 558491. [DOI] [PMC free article] [PubMed] [Google Scholar]
  58. Lundblad, L. C. , Olausson H., Wasling P., et al. 2020. “Tactile Direction Discrimination in Humans After Stroke.” Brain Communications 2, no. 2: fcaa088. [DOI] [PMC free article] [PubMed] [Google Scholar]
  59. Lupescu, I. C. , Dulamea A. O., Anghel D., et al. 2020. “The Palmomental Reflex—Overview and Clinical Significance.” Romanian Journal of Neurology 19, no. 3: 141. [Google Scholar]
  60. Lusins, J. O. , and Bender M. B.. 1973. “The Brachio‐Mental Reflex.” European Neurology 10, no. 1: 56–64. [DOI] [PubMed] [Google Scholar]
  61. Mandelbaum, R. , and Marks D. S.. 2020. “What Is Causing This Patient's Balance and Speech Problems?” Jaapa 33, no. 11: 55–57. [DOI] [PubMed] [Google Scholar]
  62. Mantel, T. , Meindl T., Li Y., et al. 2017. “Network‐Specific Resting‐State Connectivity Changes in the Premotor‐Parietal Axis in Writer's Cramp.” NeuroImage. Clinical 17: 137–144. [DOI] [PMC free article] [PubMed] [Google Scholar]
  63. Martello, J. M. 2023. “Persistent Primitive Reflex and Developmental Delay in the School‐Aged Child.” Journal for Nurse Practitioners 19, no. 10: 104767. [Google Scholar]
  64. Marterer‐Travniczek, A. , Danielczyk W., Müller F., Simanyi M., and Fischer P.. 1992. “Release Signs in Parkinson's Disease With and Without Dementia.” Journal of Neural Transmission: Parkinson's Disease and Dementia Section 4, no. 3: 207–212. [DOI] [PubMed] [Google Scholar]
  65. Mattson, M. P. 2023. Sculptor and Destroyer: Tales of Glutamate—The Brain's Most Important Neurotransmitter. Cambridge, MA: MIT Press. [Google Scholar]
  66. Matuszkiewicz, M. , and Gałkowski T.. 2021. “Developmental Language Disorder and Uninhibited Primitive Reflexes in Young Children.” Journal of Speech, Language, and Hearing Research 64, no. 3: 935–948. [DOI] [PubMed] [Google Scholar]
  67. Melillo, R. , Leisman G., Machado C., et al. 2022. “Retained Primitive Reflexes and Potential for Intervention in Autistic Spectrum Disorders.” Frontiers in Neurology 13: 922322. [DOI] [PMC free article] [PubMed] [Google Scholar]
  68. Melillo, R. J. , Leisman G., Machado C., and Carmeli E.. 2023. “Identification and Reduction of Retained Primitive Reflexes by Sensory Stimulation in Autism Spectrum Disorder: Effects on qEEG Networks and Cognitive Functions.” BMJ Case Reports 16, no. 12: e255285. [DOI] [PMC free article] [PubMed] [Google Scholar]
  69. Miles, S. R. , Hammond F. M., Neumann D., et al. 2021. “Evolution of Irritability, Anger, and Aggression After Traumatic Brain Injury: Identifying and Predicting Subgroups.” Journal of Neurotrauma 38, no. 13: 1827–1833. [DOI] [PMC free article] [PubMed] [Google Scholar]
  70. Modrell, A. K. , and Tadi P.. 2023. “Primitive Reflexes.” In StatPearls. StatPearls Publishing. [PubMed] [Google Scholar]
  71. Morningstar, M. W. , Pettibon B. R., Schlappi H., et al. 2005. “Reflex Control of the Spine and Posture: A Review of the Literature From a Chiropractic Perspective.” Chiropractic and Osteopathy 13: 1–17. [DOI] [PMC free article] [PubMed] [Google Scholar]
  72. Moura, J. , Oliveira V., Sardoeira A., et al. 2023. “Rapidly Progressive Corticobasal Degeneration Mimicking Brainstem Encephalitis.” Movement Disorders Clinical Practice 10, no. 2: 300–306. [DOI] [PMC free article] [PubMed] [Google Scholar]
  73. Nicholson, G. , and Pereira A. C.. 2002. “Parkinson's Disease and Anaesthesia.” In Bradley's Neurology in Clinical Practice E‐Book, edited by Hall G. M., 904–916. [DOI] [PubMed] [Google Scholar]
  74. Niedermeyer, E. 1998. “Frontal Lobe Functions and Dysfunctions.” Clinical EEG (Electroencephalography) 29, no. 2: 79–90. [DOI] [PubMed] [Google Scholar]
  75. Noda, K. , Kawajiri S., Tomizawa Y., Hattori N., and Okuma Y.. 2015. “Pisa Syndrome in Progressive Supranuclear Palsy: A Case Report.” Parkinsonism and Related Disorders 21, no. 9: 1115–1116. [DOI] [PubMed] [Google Scholar]
  76. Novak, M. J. U. , and Tabrizi S. J.. 2011. “Huntington's Disease: Clinical Presentation and Treatment.” International Review of Neurobiology 98: 297–323. [DOI] [PubMed] [Google Scholar]
  77. Okuda, B. , Kawabata K., Tachibana H., et al. 2008. “Primitive Reflexes Distinguish Vascular Parkinsonism From Parkinson's Disease.” Clinical Neurology and Neurosurgery 110, no. 6: 562–565. [DOI] [PubMed] [Google Scholar]
  78. Oli, K. K. , and Shrestha A.. 2024. “Coma and Vegetative State.” In Case‐Based Approach to Common Neurological Disorders, 287–296. Singapore: Springer Nature Singapore. [Google Scholar]
  79. Owen, G. , and Mulley G. P.. 2002. “The Palmomental Reflex: A Useful Clinical Sign?” Journal of Neurology, Neurosurgery, and Psychiatry 73, no. 2: 113–115. [DOI] [PMC free article] [PubMed] [Google Scholar]
  80. Paulson, G. W. , and Gottlieb G.. 1968. “Development Reflexes: The Reappearance of Foetal and Neonatal Reflexes in Aged Patients.” Brain 91, no. 1: 37–52.5643282 [Google Scholar]
  81. Pecuch, A. , Gieysztor E., Wolańska E., et al. 2021. “Primitive Reflex Activity in Relation to Motor Skills in Healthy Preschool Children.” Brain Sciences 11, no. 8: 967. [DOI] [PMC free article] [PubMed] [Google Scholar]
  82. Peddireddy, A. , Wang K., Svensson P., and Arendt‐Nielsen L.. 2006. “Influence of Age and Gender on the Jaw‐Stretch and Blink Reflexes.” Experimental Brain Research 171, no. 4: 530–540. [DOI] [PubMed] [Google Scholar]
  83. Polunina, A. G. 2011. “Postoperative Delirium: Cerebral Microemboli as a Major Etiological Factor, and Neurological Mechanisms of Psychotic Symptoms.” In Delirium: Causes, Diagnosis and Treatment, 1–48. Hauppauge, NY: Nova Science Publishers. [Google Scholar]
  84. Prajjwal, P. , Shashank S., Al‐Ezzi S. M. S., et al. 2023. “Frontotemporal Dementia: Addressing the Scattered Harbingers of Genetics and Its Relationship With Glucose Metabolism, Bipolar Disorder, and Amyotrophic Lateral Sclerosis.” Disease‐a‐Month 69, no. 5: 101545. [DOI] [PubMed] [Google Scholar]
  85. Ragab, A. , Ibrahim A., Helal R., et al. 2021. “Pharmacotherapy of Multiple Sclerosis and Treatment Strategies.” Frontiers in Clinical Drug Research‐CNS and Neurological Disorders 9: 206. [Google Scholar]
  86. Rao, R. , Jackson S., and Howard R.. 1999. “Primitive Reflexes in Cerebrovascular Disease: A Community Study of Older People With Stroke and Carotid Stenosis.” International Journal of Geriatric Psychiatry 14, no. 11: 964–972. [PubMed] [Google Scholar]
  87. Reis, D. J. 1961. “The Palmomental Reflex. A Fragment of a General Nociceptive Skin Reflex: A Physiological Study in Normal Man.” Archives of Neurology 4: 486–498. [DOI] [PubMed] [Google Scholar]
  88. Rosenbohm, A. , Kassubek J., Weydt P., et al. 2014. “Can Lesions to the Motor Cortex Induce Amyotrophic Lateral Sclerosis?.” Journal of Neurology 261: 283–290. [DOI] [PubMed] [Google Scholar]
  89. Sabayan, B. , Jansen S., Oleksik A. M., et al. 2012. “Cerebrovascular Hemodynamics in Alzheimer's Disease and Vascular Dementia: A Meta‐Analysis of Transcranial Doppler Studies.” Ageing Research Reviews 11, no. 2: 271–277. [DOI] [PubMed] [Google Scholar]
  90. Sanchez‐Ramos, J. R. , Ortoll R., and Paulson G. W.. 1996. “Visual Hallucinations Associated With Parkinson Disease.” Archives of Neurology 53, no. 12: 1265–1268. [DOI] [PubMed] [Google Scholar]
  91. Schott, J. M. , and Rossor M. N.. 2016. “The Palmomental Reflex: Stop Scratching Around!” Practical Neurology 16, no. 6: 500–501. [DOI] [PubMed] [Google Scholar]
  92. Shahed, J. , and Jankovic J.. 2007. “Motor Symptoms in Parkinson's Disease.” Handbook of Clinical Neurology 83: 329–342. [DOI] [PubMed] [Google Scholar]
  93. Shargorodsky, J. , Lin H. W., and Gopean Q.. 2010. “Facial Nerve Palsy in the Pediatric Population.” Clinical Pediatrics 49, no. 5: 411–417. [DOI] [PubMed] [Google Scholar]
  94. Sigafoos, J. , Roche L., O'Reilly M. F., et al. 2021. “Persistence of Primitive Reflexes in Developmental Disorders.” Current Developmental Disorders Reports 8: 98–105. [Google Scholar]
  95. Spreen, O. , and Risser A. H.. 2003. Assessment of Aphasia. Oxford: Oxford University Press. [Google Scholar]
  96. Sucksdorff, M. , Matilainen M., Tuisku J., et al. 2020. “Brain TSPO‐PET Predicts Later Disease Progression Independent of Relapses in Multiple Sclerosis.” Brain 143, no. 11: 3318–3330. [DOI] [PMC free article] [PubMed] [Google Scholar]
  97. Swapna, N. , Kumar P., Kalam B. R., et al. 2020. “Diagnostic Relevance of Primitive Reflexes in High‐Risk Newborns: A Systematic Review.” Journal of Indian Speech Language and Hearing Association 34, no. 1: 24–30. [Google Scholar]
  98. Swash, M. , Burke D., Turner M. R., et al. 2020. “Occasional Essay: Upper Motor Neuron Syndrome in Amyotrophic Lateral Sclerosis.” Journal of Neurology, Neurosurgery and Psychiatry 91, no. 3: 227–234. [DOI] [PubMed] [Google Scholar]
  99. Tankisi, H. , Nielsen C. S. Z., Howells J., et al. 2021. “Early Diagnosis of Amyotrophic Lateral Sclerosis by Threshold Tracking and Conventional Transcranial Magnetic Stimulation.” European Journal of Neurology 28, no. 9: 3030–3039. [DOI] [PMC free article] [PubMed] [Google Scholar]
  100. Thomas, R. J. 1994. “Blinking and the Release Reflexes: Are They Clinically Useful?” Journal of the American Geriatrics Society 42, no. 6: 609–613. [DOI] [PubMed] [Google Scholar]
  101. Thompson, A. E. , and Thompson P. D.. 2023. “Frontal Lobe Motor Syndromes.” Handbook of Clinical Neurology 196: 443–455. [DOI] [PubMed] [Google Scholar]
  102. Ticku, H. , Fotedar N., Juncos J., et al. 2022. “Pseudonystagmus in Progressive Supranuclear Palsy.” Journal of the Neurological Sciences 434: 120157. [DOI] [PubMed] [Google Scholar]
  103. Touwen, B. C. 1995. “The Neurological Development of Prehension: A Developmental Neurologist's view.” International Journal of Psychophysiology 19, no. 2: 115–127. [DOI] [PubMed] [Google Scholar]
  104. Tsuyusaki, Y. , Sakakibara R., Tateno F., et al. 2016. “Multiple System Atrophy Presenting Initially as Spastic Paraparesis.” Journal of the Neurological Sciences 360: 176–178. [DOI] [PubMed] [Google Scholar]
  105. Vallar, G. 2020. “The Methodological Foundations of Neuropsychology.” In Handbook of Clinical and Experimental Neuropsychology, edited by Vallar G., 95–132. London: Psychology Press. [Google Scholar]
  106. Van Gijn, J. 1977. “The Babinski Sign and the Pyramidal Syndrome.” Journal of Neurology, Neurosurgery and Psychiatry 40, no. 2: 180–181. [DOI] [PMC free article] [PubMed] [Google Scholar]
  107. Vidovic, M. , Aust E., Hermann A., et al. 2021. “The Palmomental Reflex in Amyotrophic Lateral sclerosis—A Clinical Sign of Executive or Motor Dysfunction?” Amyotrophic Lateral Sclerosis and Frontotemporal Degeneration 22, no. 7–8: 588–591. [DOI] [PubMed] [Google Scholar]
  108. Vreeling, F. W. 1994. “De Betekenis Van Primitieve Reflexen Bij Volwassenen [The Significance of Primitive Reflexes in Adults].” Ned Tijdschr Geneeskd 138, no. 36: 1798–1803. [PubMed] [Google Scholar]
  109. Vreeling, F. W. , Verhey F. R., Houx P. J., et al. 1993. “Primitive Reflexes in Parkinson's Disease.” Journal of Neurology, Neurosurgery and Psychiatry 56, no. 12: 1323–1326. [DOI] [PMC free article] [PubMed] [Google Scholar]
  110. Wallace, E. R. , Harp J. P., Van Pelt K. L., et al. 2021. “Identifying Dementia in Down Syndrome With the Severe Impairment Battery, Brief Praxis Test and Dementia Scale for People With Learning Disabilities.” Journal of Intellectual Disability Research 65, no. 12: 1085–1096. [DOI] [PMC free article] [PubMed] [Google Scholar]
  111. Walterfang, M. , and Velakoulis D.. 2005. “Cortical Release Signs in Psychiatry.” Australian and New Zealand Journal of Psychiatry 39, no. 5: 317–327. [DOI] [PubMed] [Google Scholar]
  112. Walther, S. , Vanbellingen T., Müri R., et al. 2013. “Impaired Gesture Performance in Schizophrenia: Particular Vulnerability of Meaningless Pantomimes.” Neuropsychologia 51, no. 13: 2674–2678. [DOI] [PubMed] [Google Scholar]
  113. Whittle, I. R. , and Miller J. D.. 1987. “Clinical Usefulness of the Palmomental Reflex.” Medical Journal of Australia 146, no. 3: 137–139. [DOI] [PubMed] [Google Scholar]
  114. Wibawa, P. , O'Connor R., Kenchaiah B., et al. 2023. “Motor Neuron Disease & Frontotemporal Dementia Presenting With a Conversion Disorder.” Psychiatry Research Case Reports 2, no. 1: 100082. [Google Scholar]
  115. Wijdicks, E. F. M. 2021. “Unraveling Unconsciousness.” In Examining Neurocritical Patients, edited by Wijdicks E. F. M., 103–118. Oxford: Oxford University Press. [Google Scholar]
  116. Xu, Y. , Li Y., Richard S. A., et al. 2024. “Genetic Pathways in Cerebral Palsy: A Review of the Implications for Precision Diagnosis and Understanding Disease Mechanisms.” Neural Regeneration Research 19, no. 7: 1499–1508. [DOI] [PMC free article] [PubMed] [Google Scholar]
  117. Yadav, R. , Mahale R., and Pal P. K.. 2018. “Palmomental Reflex Is an Important Clinical Marker of REM Sleep Behavior Disorder in Patients With Parkinson's Disease.” Annals of Movement Disorders 1, no. 1: 44–48. [Google Scholar]
  118. Zafeiriou, D. I. 2004. “Primitive Reflexes and Postural Reactions in the Neurodevelopmental Examination.” Pediatric Neurology 31, no. 1: 1–8. [DOI] [PubMed] [Google Scholar]
  119. Zafeiriou, D. I. , Tsikoulas I. G., and Kremenopoulos G. M.. 1995. “Prospective Follow‐Up of Primitive Reflex Profiles in High‐Risk Infants: Clues to an Early Diagnosis of Cerebral Palsy.” Pediatric Neurology 13, no. 2: 148–152. [DOI] [PubMed] [Google Scholar]
  120. Zanoni, P. , Steindl K., Sticht H., et al. 2023. “The Genetic Landscape and Clinical Implication of Pediatric Moyamoya Angiopathy in an International Cohort.” European Journal of Human Genetics 31, no. 7: 784–792. [DOI] [PMC free article] [PubMed] [Google Scholar]
  121. Zhang, S. , Wang Y., Liu L., et al. 2021. “Case Report of a Pathologically Confirmed Vascular Parkinsonism With Early Cognitive Impairment and Behavioral Disturbance.” BMC Neurology 21: 1–6. [DOI] [PMC free article] [PubMed] [Google Scholar]

Associated Data

This section collects any data citations, data availability statements, or supplementary materials included in this article.

Data Availability Statement

All data generated or analyzed during this study are included in this published article.


Articles from Brain and Behavior are provided here courtesy of Wiley

RESOURCES