Cortical Taste Area Research Articles

The Bitter Touch: Acquired Tactile-Gustatory Synesthesia

AbstractIntroductionGustatory sensation in response to tactile stimulation has been reported to occur in only 0.6% of synesthetes and has rarely been formally described.MethodsCase Study: A 29-year-old female with schizoaffective disorder – depressed subtype, two months prior to presentation, began noticing that when she touched objects, she would experience an abnormal taste in her mouth. When she would touch specific items with her fingertips, for instance wood, bedsheets, tables, cups, plates, silverware, metal, trash cans, and toothpaste would induce a bitter taste. Touching wood caused the most intense bitter taste. Touching glass did not precipitate a taste.ResultsMental Status Examination: Disheveled and guarded with minimal eye contact. Anxious and agitated. She believes people are stalking her and that cell phones, radios, and computers emit radiation which makes her head burn as if it is on fire. She perceived that inanimate objects, such as furniture, were staring at her. Other: CT scan of brain with and without contrast: normal.DiscussionThis could be due to neural overactivation between brain regions due to a neighborhood effect, with cross-firing of connecting fibers. The cortical taste area of the brain lies within the Brodmann area 43 of the parietal lobe which includes the pre- as well as post-central gyri extending into the parietal operculum. Brodmann areas 3, 1, and 2 in the postcentral gyrus is where the primary sensation for touch is mediated. The stimulation in adjacent and overlapping anatomical structures may be explained by ephaptic transmission with firing of one causing discharge of the second, yclept the adjacency principle.This co-localization hypothesis is further supported by the occurrence of pathological state of seizures which manifest both tactile and gustatory sensation. Such a hypothesis would be supported by Anderson’s 1886 observation discussing a peculiar sensation in the right arm and hand elicited concurrently with a bitter sensation in the mouth. Through an overflow phenomenon, touch may induce a diffuse serotonergic discharge to more remote regions of the brain that may mediate their functions through serotonin, such as taste. Possibly, other pathology may be invoked to explain this synesthesia. A deprived sensory system may be hyper-receptive to stray or overflow of sensations which are then interpreted within the sensorily deprived sensory system, as in Charles Bonnet syndrome. In the chemosensory sphere, sensory deprivation is associated with chemosensory hallucinations. If the patient manifests gustatory deficit, it may have predisposed her to sensitivity to such stray or overflowing sensory stimulus from touch manifesting as gustation. In those who present with synesthesia, investigation of pathology in the sensory system of the receiving concurrent sensation is warranted.FundingNo Funding

Prandial States Modify the Reactivity of the Gustatory Cortex Using Gustatory Evoked Potentials in Humans.

Previous functional Magnetic Resonance Imaging studies evaluated the role of satiety on cortical taste area activity and highlighted decreased activation in the orbito-frontal cortex when food was eaten until satiation. The modulation of orbito-frontal neurons (secondary taste area) by ad libitum food intake has been associated with the pleasantness of the food's flavor. The insula and frontal operculum (primary taste area) are also involved in reward processing. The aim was to compare human gustatory evoked potentials (GEP) recorded in the primary and secondary gustatory cortices in a fasted state with those after food intake. Fifteen healthy volunteers were enrolled in this observational study. In each of two sessions, two GEP recordings were performed (at 11:00 am and 1:30 pm) in response to sucrose gustatory stimulation, and a sucrose-gustatory threshold was determined. During one session, a standard lunch was provided between the two GEP recordings. During the other session, subjects had nothing to eat. Hunger sensation, wanting, liking, and the perception of the solution's intensity were evaluated with visual analog scales. GEP latencies measured in the Pz (p < 0.001), Cz (p < 0.01), Fz (p < 0.001) recordings (primary taste area) were longer after lunch than in the pre-prandial condition. Fp1 and Fp2 latencies (secondary taste area) tended to be longer after lunch, but the difference was not significant. No difference was observed for the sucrose-gustatory threshold regardless of the session and time. Modifications in the primary taste area activity during the post-prandial period occurred regardless of the nature of the food eaten and could represent the activity of the frontal operculum and insula, which was recently shown to be modulated by gut signals (GLP-1, CCK, ghrelin, or insulin) through vagal afferent neurons or metabolic changes of the internal milieu after nutrient absorption. This trial was registered at clinicalstrials.gov as NCT02472444.

Altered Taste and Stroke: A Case Report and Literature Review

Patients with altered taste perception following stroke are at risk for malnutrition and associated complications that may impede recovery and adversely affect quality of life. Such deficits often induce and exacerbate depressive symptomatology, which can further hamper recovery. It is important for clinicians and rehabilitation specialists to monitor stroke patients for altered taste perception so that this issue can be addressed. The authors present the case of a patient who experienced an isolated ischemic infarct affecting a primary cortical taste area. This case is unusual in that the isolated injury allowed the patient to remain relatively intact cognitively and functionally, and thus able to accurately describe her taste-related deficits. The case is further used to describe the relevant neurological taste pathways and review potential taste-related therapies.

Altered Taste and Stroke: A Case Report and Literature Review

Patients with altered taste perception following stroke are at risk for malnutrition and associated complications that may impede recovery and adversely affect quality of life. Such deficits often induce and exacerbate depressive symptomatology, which can further hamper recovery. It is important for clinicians and rehabilitation specialists to monitor stroke patients for altered taste perception so that this issue can be addressed. The authors present the case of a patient who experienced an isolated ischemic infarct affecting a primary cortical taste area. This case is unusual in that the isolated injury allowed the patient to remain relatively intact cognitively and functionally, and thus able to accurately describe her taste-related deficits. The case is further used to describe the relevant neurological taste pathways and review potential taste-related therapies.

Bidirectional lexical–gustatory synesthesia

In developmental lexical-gustatory synesthesia, specific words (inducers) can trigger taste perceptions (concurrents) and these synesthetic associations are generally stable. We describe a case of multilingual lexical-gustatory synesthesia for whom some synesthesias were bidirectional as some tastes also triggered auditory word associations. Evoked concurrents could be gustatory but also tactile sensations. In addition to words and pseudowords, many voices were effective inducers, suggesting increased connections between cortical taste areas and both voice-selective and language-selective areas. Lasting changes in some evoked tastes occurred during childhood suggesting that some plasticity can be present after the initial learning of associations. Inducers were often linked to taste concurrents phonologically or semantically, but also through identifiable childhood episodes (persons or events). Several inducers were phonologically linked to episodic inducers suggesting a process of secondary acquisition for many inducers. Implications of these observations are discussed.

Human cortical representation of oral temperature

The temperature of foods and fluids is a major factor that determines their pleasantness and acceptability. Studies of nonhuman primates have shown that many neurons in cortical taste areas receive and process not only chemosensory inputs, but oral thermosensory (temperature) inputs as well. We investigated whether changes in oral temperature activate these areas in humans, or middle or posterior insular cortex, the areas most frequently identified for the encoding of temperature information from the human hand. In the fMRI study we identified areas of activation in response to innocuous, temperature-controlled (cooled and warmed, 5, 20 and 50 °C) liquid introduced into the mouth. The oral temperature stimuli activated the insular taste cortex (identified by glucose taste stimuli), a part of the somatosensory cortex, the orbitofrontal cortex, the anterior cingulate cortex, and the ventral striatum. Brain regions where activations correlated with the pleasantness ratings of the oral temperature stimuli included the orbitofrontal cortex and pregenual cingulate cortex. We conclude that a network of taste- and reward-responsive regions of the human brain is also activated by intra-oral thermal stimulation, and that the pleasant subjective states elicited by oral thermal stimuli are correlated with the activations in the orbitofrontal cortex and pregenual cingulate cortex. Thus the pleasantness of oral temperature is represented in brain regions shown in previous studies to represent the pleasantness of the taste and flavour of food. Bringing together these different oral representations in the same brain regions may enable particular combinations to influence the pleasantness of foods.

Chemotopic Arrangement for Taste Quality Discrimination in the Cortical Taste Area

Signals from various sensory organs are delivered to the brain where sensory information is generated from the signals. The information is represented on the brain in the form of temporal and spatial codes, which enable us to create inner an representation of the outer world (Florey, 1990). In the neocortex, the information consisting of the spatial codes is principally arranged in the primary sensory area as a receptive field, by way of anatomical column formation. The information consisting of temporal codes, such as frequency and phase dynamics, also plays an important role for synchronization of neural activities or strengthening signal amplitudes. Interaction or integration of the information by way of intra-cortical or cortico-cortical connections enables the temporal and spatial codes to link (Singer and Gray, 1995; Gilbert et al., 1996; Salinas and Sejnowski, 2001). As for taste information processing, controversy still exists as to whether cortical taste neurons use temporal codes or spatial codes for discriminating taste information in the cortical taste area. However, it may be presumed that cortical taste neurons use spatial codes as well as frequency codes in order to discriminate taste information efficiently. Previous electrophysiological studies predict that there is a chemotopic arrangement for taste quality discrimination in the cortical taste area, but this hypothesis has not been confirmed because of lacking for the evidence with high resolution of spatial dimension. Optical imaging based on intrinsic signals has a high spatial resolution (Frostig et al., 1990) and is useful for studying the functional organization of the brain (Bonhoeffer and Grinvald, 1996). Here, we investigated the spatial aspects of optical intrinsic signal (OIS) responses in the gustatory insular cortex that were elicited by delivering a solution of tastants on the tongue.

P.6.065 Anti-stigma projects against the discrimination of psychiatric patients. A literature search and a world-wide survey

To investigate the neural encoding of glutamate taste in the primate, recordings were made from taste responsive neurons in the cortical taste areas in macaques. Most of the neurons were in the orbitofrontal cortex taste area, with a small number in adjacent taste areas. First, it was shown that single neurons that had their best responses to sodium glutamate also had good responses to glutamic acid. The correlation between the responses to these two tastants was higher than between any other pair of tastants, which included glucose (sweet), sodium chloride (salty), HCl (sour), and quinine HCl (bitter). Accordingly, the responsiveness to glutamic acid clustered with the response to monosodium glutamate in a cluster analysis with this set of stimuli, and glutamic acid was close to sodium glutamate in a space created by multidimensional scaling. Second, it was shown that the responses of these neurons to the nucleotide umami tastant inosine 5′-monophosphate were more correlated with their responses to monosodium glutamate than to any prototypical tastant. Third, concentration response curves showed that concentrations of monosodium glutamate as low as 0.001 M were just above threshold for some of these neurons. Fourth, neurons have not yet been found in this cortical region that showed synergism of monosodium glutamate and the nucleotide inosine 5′-monophosphate: it was shown that mixtures of 0.0001 M inosine 5′-monophosphate with different concentrations (0.001, 0.01, and 0.1 M) of monosodium glutamate did not have a greater effect than the monosodium glutamate alone. Fifth, some neurons in the orbitofrontal region, which responded to monosodium glutamate and other food tastes, decreased their responses after feeding with monosodium glutamate to behavioural satiety. In some cases this reduction was sensory-specific. These findings show that the taste neurons activated by monosodium glutamate can also be activated by other umami tastants, including glutamic acid and the nucleotide inosine 5′-monophosphate. The responses to these umami tastants were more similar to each other than to any of the other prototypical tastant, providing evidence that in this system umami is encoded differently from the other tastants. Moreover, the findings with these tastants provide additional evidence that the responses to monosodium glutamate are not due just to activation of a sodium taste channel.

Cortical spatial aspects of optical intrinsic signals in response to sucrose and NaCl stimuli.

To examine whether cortical taste neurons use spatial codes for discriminating taste information, we investigated the spatial aspects of optical intrinsic signal (OIS) responses in the gustatory insular cortex (GC) elicited by the administration of two essential tastants, sucrose and NaCl, on the tongue. OIS responses to sucrose appeared in the rostral part of the GC, whereas those to NaCl appeared in the central part of the GC. Local anesthetization of the tongue abolished OIS responses, and the administration of distilled water elicited no OIS response. Thus, taste information elicited by sucrose and NaCl from the peripheral sensory organs is segregated in the GC, suggesting that the information from two essential tastants is assembled as spatial codes in the primary cortical taste area through the process of taste quality perception.

Responsiveness of the cortical taste area neurons to a mixture of the four basic tastants in rats.

The taste coding mechanism in the cortical taste area was investigated by analyzing the responses of 59 neurons in the cortical taste area of the anesthetized rat to a mixture of the four basic tastants in both absence and presence of bicuculline methiodide, a specific antagonist to the GABA(A) receptors. The mixture caused response suppression more frequently than response facilitation, both in the control state and during bicuculline application. Cluster analysis revealed that only a group of the neurons with the best response to both NaCl and HCl (group NH) showed the best response to the mixture in the control state, whereas during bicuculline application, in addition to group NH, two other groups of neurons responding to sucrose, or to HCl and quinine responded vigorously to the mixture. Multidimensional scaling located the mixture outside the space of the four basic tastants facing an NaCl-HCl line in both states. GABAergic inhibition caused the group NH to represent the taste of the mixture in the control state. Thus, the mixture probably tastes salty and sour to rats. No cortical neuron was found which specifically responded to the mixture.

Columnar organization of mechanoreceptive neurons in the cortical taste area in the rat.

Mechanoreceptive neurons with or without taste responsiveness were recorded in the cortical taste area (CTA) of rats every 50 or 100 micro m along an electrode track made as perpendicular to the surface as possible. Three groups of mechanoreceptive neurons were recognized based on the adequate stimulus, i.e., low-threshold mechanoreceptive ( n=16), nociceptive-specific ( n=48), and wide-dynamic range neurons ( n=392). Except for nine neurons, almost all had receptive fields (RFs) in the oral cavity ( n=447). They were categorized into three RF types: those with RFs only in the oral cavity (OC type; n=23), those with RFs both in the oral cavity and on the lip (OL type; n=44) and those with RFs in the oral cavity and on the external surface of the body (WB type; n=380), e.g., tail. Neurons with inhibitory RFs were often located in the infragranular layers. Several neurons with the same receptive features were sequentially recorded along the track, suggesting the presence of columnar organization. The diameter of the possible functional column was the largest (mean 113.85 micro m) for WB type neurons, but smaller in the other two types (mean 85 micro m for the OC type and 62.5 micro m for the OL type). Neurons were segregated according to the adequate stimulus within the column for WB type neurons. Taste-responsive mechanoreceptive neurons ( n=33) were recorded at 15 tracks, and two taste neurons were sequentially recorded in five cases, in three of which two successive neurons sharing the best stimulus were recorded. Taste neurons are possibly arranged in a column with a very small diameter within the large column of mechanoreceptive neurons.

Neurons in the cortical taste area receive nociceptive inputs from the whole body as well as the oral cavity in the rat

Almost all mechanoreceptive neurons in the cortical taste area (CTA) of the rat had receptive fields (RFs) in the oral cavity, except for a few neurons at the border with the primary somatosensory area that had RFs on the contralateral rhinarium or upper lip. About one-third of the mechanoreceptive neurons with RFs in the oral cavity had additional RFs on the tips of limbs, earflaps or tail, i.e. the glabrous skin or skin with sparse hairs of the external surface of the body (whole body type). Most of these neurons received both innocuous and noxious inputs (wide dynamic range type), but some had either type of input (low threshold mechanoreceptive or nociceptive specific type). Some nociceptive neurons were responsive to taste, as previously found. Nociceptive neurons with the whole body type of RFs were diffusely distributed across the CTA without clustering. The corticocortical afferents, probably originating from the visceral part of the insula, may code body condition to modulate the taste responsiveness of the cortical taste neurons.

Callosal connections of the cortical taste area in rats

The granular and dysgranular insular subregions of the cortical taste area in rats are shown to connect anatomically with the homotopical regions in the opposite hemisphere through the corpus callosum. Cells of callosal efferents and terminals of callosal fibers were found in almost all cortical layers. The findings clarify the current understanding of the morphological substrate of callosal interactions in the gustatory system.

The representation of umami taste in the human and macaque cortex

To investigate the neural encoding of glutamate (umami) taste in the primate, recordings were made from taste responsive neurons in the cortical taste areas in macaques. Most of the neurons were in the orbitofrontal cortex (secondary) taste area. First, it was shown that there is a representation of the taste of glutamate which is separate from the representation of the other prototypical tastants sweet (glucose), salt (NaCl), bitter (quinine) and sour (HCl). Second, it was shown that single neurons that had their best responses to sodium glutamate also had good responses to glutamic acid. Third, it was shown that the responses of these neurons to the nucleotide umami tastant inosine 5′-monophosphate were more correlated with their responses to monosodium glutamate than to any prototypical tastant. Fourth, concentration-response curves showed that concentrations of monosodium glutamate as low as 0.001 M were just above threshold for some of these neurons. Fifth, some neurons in the orbitofrontal region, which responded to monosodium glutamate and other food tastes, decreased their responses after feeding with monosodium glutamate to behavioural satiety, revealing a mechanism of satiety. In some cases this reduction was sensory-specific. Sixth, it was shown in psychophysical experiments in humans that the flavor of umami is strongest with a combination of corresponding taste and olfactory stimuli (e.g. monosodium glutamate and garlic odor). The hypothesis is proposed that part of the way in which glutamate works as a flavor enhancer is by acting in combination with corresponding food odors. The appropriate associations between the odor and the glutamate taste may be learned at least in part by olfactory to taste association learning in the primate orbitofrontal cortex. Seventh, in neuroimaging experiments with functional magnetic resonance imaging (fMRI) in humans, it was shown that in humans umami taste produced by monosodium glutamate or by inosine monophosphate produced activation in a region of the anterior insula which is the putative human primary taste cortex and in a part of the orbitofrontal cortex which is the putative human secondary taste cortex.

Effects of reversible block of callosal afferent inputs on the response characteristics of single neurons in the cortical taste area in rats.

We examined the change in magnitude of the taste responses of single neurons in the cortical taste area (CTA) in one side by reversibly blocking the CTA in the other side with a local anesthetic, procaine-HCl, in urethane-anesthetized rats. Taste responses of 68 taste neurons were continuously recorded for up to 2 h until recovery from the treatment, and those in 50 of them were found to be affected significantly. No remarkable difference was noted in the spatial distribution of the affected and non-affected neurons in the CTA. Many of the affected neurons were located in layers IV and V of area GI and in layer V of area DI. In most cases, changes in the taste responses of single neurons were in one direction, i.e., either a decrease or an increase, but in a few cases they decreased or increased depending on the stimulus. The taste profile of callosal inputs was estimated by subtracting responses after treatment from the control responses before treatment. The results suggest that the CTAs on both sides are functionally connected by way of callosal fibers as anatomical studies indicate, and that the CTA in one side receives excitatory or inhibitory inputs from the other side.

Action of calcitonin gene-related peptide (CGRP) and substance P on neurons in the insular cortex and the modulation of taste responses in the rat.

Using multibarrel electrodes, recordings were made from single neurons in the insular cortex including the cortical taste area (CTA) of urethane-anesthetized rats. The effects of an iontophoretic application of calcitonin gene-related peptide (CGRP) and substance P (SP) on the spontaneous discharges and taste responses were tested. In a total sample of neurons (mostly non-taste), CGRP affected the spontaneous discharges in 35.6% of the 571 neurons studied and SP in 38.3% of the 775 neurons studied. The effects were mostly (approximately 85-87%) facilitatory. Peptide-sensitive neurons were found at a similar frequency in all three insular areas-granular, dysgranular and agranular (areas GI, DI and AI). This is in contrast to previous reports that CGRP receptors were rich in area DI and CGRP-immunoreactive afferents numerous in area AI, but consistent with previous reports that the distribution of SP receptors and SP fibers was dense in the insular cortex. In approximately 40% of the 76 taste neurons recorded from areas GI and DI, the peptides affected the spontaneous discharges (mostly facilitated). When the taste responses were examined during application of the peptides, significant (mainly depressant) effects were seen in 61% of 18 neurons for CGRP and in 70.5% of 17 for SP. Such effects were not recognized on responses to specific taste stimuli and were not correlated with the effects on the spontaneous discharges. The findings indicate that both peptides modify taste coding in CTA neurons presynaptically and/or postsynaptically, independently of the existence of receptors on the neurons.

The Representation of Umami Taste in the Taste Cortex

To investigate the neural encoding of glutamate (umami) taste in the primate, recordings were made from taste-responsive neurons in the cortical taste areas in macaques. Most of the neurons were in the orbitofrontal cortex (secondary) taste area. First, it was shown that there is a representation of the taste of glutamate that is separate from the representation of the other prototypical tastants, sweet (glucose), salt (NaCl), bitter (quinine) and sour (HCl). Second, it was shown that single neurons that had their best responses to sodium glutamate also had good responses to glutamic acid. Third, it was shown that the responses of these neurons to the nucleotide umami tastant inosine 5'-monophosphate were more correlated with their responses to monosodium glutamate than to any prototypical tastant. Fourth, concentration-response curves showed that concentrations of monosodium glutamate as low as 0.001 mol/L were just above threshold for some of these neurons. Fifth, some neurons in the orbitofrontal region which responded to monosodium glutamate and other food tastes, decreased their responses after feeding with monosodium glutamate to behavioral satiety, revealing a mechanism of satiety. In some cases, this reduction was sensory-specific. Sixth, it was shown in psychophysical experiments in humans that the flavor of umami is strongest with a combination of corresponding taste and olfactory stimuli (e.g., monosodium glutamate and garlic odor). The hypothesis is proposed that part of the way in which glutamate works as a flavor enhancer is by acting in combination with corresponding food odors. The appropriate associations between the odor and the glutamate taste may be learned at least in part by olfactory to taste association learning in the primate orbitofrontal cortex.

The neurophysiology of taste and olfaction in primates, and umami flavor.

To investigate the neural encoding of glutamate (umami) taste in the primate, recordings were made from taste responsive neurons in the cortical taste areas in macaques. Most of the neurons were in the orbitofrontal cortex (secondary) taste area. First, it was shown that there is a representation of the taste of glutamate which is separate from the representation of the other prototypical tastants sweet (glucose), salt (NaCl), bitter (quinine) and sour (HCl). Second, it was shown that single neurons that had their best responses to sodium glutamate also had good responses to glutamic acid. Third, it was shown that the responses of these neurons to the nucleotide umami tastant inosine 5'-monophosphate were more correlated with their responses to monosodium glutamate than to any prototypical tastant. Fourth, concentration response curves showed that concentrations of monosodium glutamate as low as 0.001 M were just above threshold for some of these neurons. Fifth, some neurons in the orbitofrontal region, which responded to monosodium glutamate and other food tastes, decreased their responses after feeding with monosodium glutamate to behavioral satiety, revealing a mechanism of satiety. In some cases this reduction was sensory-specific. Sixth, it was shown in psychophysical experiments in humans that the flavor of umami is strongest with a combination of corresponding taste and olfactory stimuli (e.g., monosodium glutamate and garlic odor). The hypothesis is proposed that part of the way in which glutamate works as a flavor enhancer is by acting in combination with corresponding food odors. The appropriate associations between the odor and the glutamate taste may be learned at least in part by olfactory to taste association learning in the primate orbitofrontal cortex.

GABAergic inhibition and modifications of taste responses in the cortical taste area in rats

Using multibarrel electrodes, recordings were made in the cortical taste area (CTA), specifically in the granular and dysgranular parts of the insular cortex (areas GI and DI), of urethane-anesthetized rats. The effects of an iontophoretic application of γ-aminobutylic acid (GABA) and bicuculline methiodide (BMI), a specific antagonist to the GABA A receptor, were tested. GABA decreased background discharges in ca. 69% of 509 neurons in both areas, and in ca. 58% of 64 taste neurons. BMI antagonized the inhibitory action of GABA in CTA neurons and facilitated background discharges in ca. 51% of the 390 neurons tested, including ca. 69% of the 52 taste neurons, which indicates that CTA neurons have GABA A receptors to receive inhibitory inputs from interneurons. In both areas, the effects of BMI (6–20 nA) on taste responses of the 85 CTA neurons (49 and 36 in areas GI and DI, respectively) to the four basic taste stimuli were examined: 65 neurons were recognized in the absence of BMI, whereas 20 only in the presence of the drug. BMI increased taste responses in 25 of the former group and changed the type of their response profiles in 25 including 12 neurons whose responses were increased. It also changed the best stimulus in 34 neurons. The drug affected the receptive fields in almost all cases examined ( n=23) and increased the size in 78.2% when the value for all four basic taste stimuli were totaled. New receptive fields were uncovered by BMI in varying regions of the oral cavity depending on the taste stimulus. But the drug decreased taste responses in several neurons ( n=8). These findings indicate that the GABAergic inhibitory system apparently contributes to modifying or selecting taste information in both areas of the CTA.

Cortical connections of the primary somatosensory cortex and cortical taste area in rats

The EU legislation requests post-market environmental monitoring (PMEM) of a genetically modified (GM) organism even if its pre-market risk assessment indicated negligible risks. It has been claimed that the monitoring of the only currently commercially cultivated GM plant in the EU, Bt MON810 maize, has not revealed any adverse effects. However, the implementation of its PMEM has been criticised repeatedly by the European Food Safety Authority (EFSA).Although EFSA agreed with the monitoring plan consisting of four tools, as proposed by the company which markets MON810, in practice PMEM has relied on famers’ questionnaires, a farmers’ complaint system, and a literature survey. The fourth approach, environmental surveillance networks, has not been utilised yet. Furthermore, PMEM requires that farmers plant a refuge of non-Bt maize in order to sustain the efficiency of the plant in combating the targeted pest.This paper aims to contribute to improved PMEM by means of a critical evaluation of its implementation in the Czech Republic based on interviews and a questionnaire survey of farmers who cultivated MON810. The results indicate that a quarter of the farmers who were surveyed did not comply with the refuge requirement. Moreover, farmers often lacked the knowledge, time, and motivation to observe and report the potential impacts of Bt maize on biodiversity, which is supposed to be monitored by the PMEM farmers’ questionnaire.The findings of this study compound the previous criticism and suggest that the current practice of PMEM limits its aim of detecting unanticipated adverse effects of MON810 maize cultivation on human and animal health and the environment. The PMEM plan should be revised before the approval process of the application for the renewal of the authorisation for MON810 cultivation in the EU continues.