Introduction
Stroke or cerebrovascular accidents (CVAs) are common causes of neurological dysfunction in dogs and can be broadly classified into two categories: ischemic and hemorrhagic. Hemorrhagic strokes result from rupture of a vessel supplying the brain parenchyma, whereas ischemic strokes result from occlusion of these vessels (1–3). In ischemic stroke, arterial occlusion triggers a cascade of pathophysiological processes that occur throughout the neural tissue irrigated by the affected vessel. This results in characteristic MRI features of ischemic infarction, commonly reported as sharply demarcated intra-axial lesions confined to a neovascular territory, that are primarily affecting the gray matter due to its comparative vulnerability to ischemia (1–4). These are typically homogeneously T2w and FLAIR hyperintense and T1w isointense or hypointense relative to adjacent neuroparenchyma, demonstrating absent, or weak enhancement on T1w post-contrast images, with a hypointense signal on apparent diffusion coefficient (ADC) maps. The latter denotes restrictive diffusion in the initial stages, becoming progressively ADC hyperintense from days 4–10 due to pseudonormalization followed by facilitative diffusion (2, 3, 5, 6). In true ischemic, also known as “pale” infarction, signal void is absent on T2*w gradient echo (GE) sequences, differentiating ischemic from hemorrhagic stroke, or ischemic stroke with hemorrhagic transition (7).
Conversely, rupture or breakdown of vascular structures seen in hemorrhagic stroke, or ischemic stroke with hemorrhagic transition, is associated with extravasation of blood into the infarcted zone, surrounding parenchyma, ventricles, subdural, or subarachnoid space leading to the development of hematoma or diffuse hemorrhagic infiltration (8). The MRI appearance of hemorrhagic stroke is largely dependent on the age of the lesion; a variable T1w and T2w intensity can be observed due to the state of oxidation of hemoglobin present and its respective magnetic properties determined by the number of unpaired outer-shell electrons of its molecular structure (9, 10). In the more chronic stages of intracranial hemorrhage, paramagnetic methemoglobin causes T1 shortening and, subsequently, a high signal on T1w images, with an associated intralesional signal void on T2*w gradient echo or susceptibility-weighted imaging sequences (SWI) (3, 10–12).
Although typically associated with hemorrhagic infarcts or ischemic infarcts with hemorrhagic transition, cases of presumed ischemic stroke with T1w hyperintense signal in absence of associated signal void on T2*w GE or susceptibility-weighted imaging (SWI) sequences have been sporadically demonstrated in human stroke patients (13–17). Although incompletely understood, these studies hypothesize that the presence of T1w hyperintense signal within non-hemorrhagic ischemic infarction is a result of incomplete tissue infarction, selective neuronal loss, or peripheral cortical laminar necrosis (6, 13, 17, 18). Histopathologically, T1w hyperintense regions within ischemic stroke lesions have been correlated with (1) focal gemistocytic astrocytosis, (2) increase in tissue protein concentration, (3) lipid deposition within macrophages, (4) tissue calcification, and (5) paramagnetic substance deposition (13, 19).
Ischemia-related T1w hyperintensities have been observed in studies of dogs with experimentally induced ischemia of the middle cerebral artery (17). In this study, an intralesional T1w hyperintensity was observed both throughout the lesion or at the lesion periphery 8 days after the onset of induced ischemia (17). However, this study lacked both assessments by gradient echo sequences and histopathology; hence, the origin of this T1w hyperintensity in the context of stroke warrants further evaluation. Cortical T1w hyperintensities are also a feature of cortical laminar necrosis, a selective polioencephalomalacia that occurs secondary to global hypoxia or hypoglycemia (20–22). This condition, however, targets the more metabolically active layers of the cerebral cortex and, hence, does not explain the T1w hyperintensity observed stroke lesions that affect structures other than the cerebral cortex. To the authors' knowledge, no studies have described non-hemorrhagic T1w hyperintense lesions specific to dogs with territorial or lacunar strokes in a clinical setting.
Considering the discrepancy in underlying pathologies caused with hemorrhagic stroke and ischemic stroke, it is important that alternative pathological processes are considered to explain the presence of T1w hyperintense signal, other than the presence of hemorrhage (5, 23). The aims of this study were 3-fold: The main aim was to investigate the presence of T1w hyperintensity in dogs with ischemic infarcts. The second aim of this study was to investigate the relationship between T1w hyperintense non-hemorrhagic infarcts and the onset of clinical signs. The third aim was to propose theories for the pathophysiology of the hyperintensity in T1w based on previous literature. It was hypothesized that first, T1w hyperintense signal would be observed without the presence of signal void in a small population of canine patients presenting with suspected CVA, and second, these lesions would be more frequently observed in the acute to subacute stages (i.e., 1–3 weeks) following the vascular event.
Materials and methods
This is a retrospective multicenter study performed across the databases of Willows Veterinary Centre and Referral Service (Solihull, UK), Ars Veterinaria Hospital (Barcelona, Spain), and Vet Oracle Teleradiology service. Due to the non-invasive and retrospective nature of this study, ethics approval was not necessary; however, consent for the use of data was obtained for all patients. Databases were searched for dogs undergoing MRI of the brain for a suspected stroke between 2013 and 2021, using keywords “stroke,” “cerebrovascular accident,” and “CVA.”
To be included in the study, dogs must have presented for the evaluation of acute or per-acute onset of focal brain dysfunction which was non-progressive after 24 h, suggestive of stroke. Only dogs that had undergone a complete MRI study of the brain and had MRI findings compatible with brain infarct were selected (Figure 1). For the purpose of this study, a complete MRI series was defined as sagittal, dorsal, and transverse image planes and a minimum of T2-weighted (T2W), transverse pre-contrast T1-weighted images (T1W), and a T2*w gradient echo sequence such as T2*w FGE or SWI. In addition, analysis of T1w post-contrast images (IV injection of 0.1 mmol of gadolinomide/kg of body weight), fluid-attenuated inversion recovery (FLAIR), and diffusion-weighted imaging (DWI) were analyzed when available. The MRI diagnosis of presumed brain infarction was made on the basis of imaging criteria previously described in dogs (5). These included intra-axial lesions that were predominantly affecting gray matter, with occasional white matter involvement if gray matter changes are severe, and confined to a neovascular territory of a main cerebral artery (rostral cerebral, middle cerebral, caudal cerebral, rostral cerebellar, caudal cerebellar, or one of their respective branches) or a perforating artery (striate arteries, perforating arteries of the caudal communicating artery, or perforating arteries of the brainstem) (2, 3, 5).
Dogs with intracranial pathologies other than suspected stroke or with evidence of intracranial signal void on T2*w GE or SWI sequences were excluded from the study. Dogs with other CSF abnormalities other than those compatible with stroke were also excluded (24).
Demographic data (age, sex, breed, and bodyweight), presenting clinical signs, and physical and neurological examination findings, as performed by the attending veterinary neurologists were recorded for each case.
Clinical findings that were documented include presence of seizures (none/isolated/cluster seizures), mentation (normal/lethargy/disorientation/depression/obtunded/stuporous), behavior (normal, altered), posture (normal/head tilt/head turn), gait (normal, ataxia, paresis/plegia) and limb(s) affected, proprioception (normal/deficits), vision (normal/unilateral or bilateral deficits), presence of cranial nerve abnormalities [normal/absent menace/absent palpebral, absent pupillary light response (PLR), absent nasal stimulation, absent gag reflex, and strabismus] and side(s) affected, hyperesthesia (yes/no), and further vestibular anomalies (none, vestibular ataxia, and nystagmus).
Cerebrospinal fluid (CSF) analysis and infectious disease analysis available were recorded. CSF findings suggestive of stroke included normal analysis results, or increased protein concentration, mild neutrophilic or mononuclear pleocytosis [30 cells/mL], xanthochromia, and hemosiderosis (5, 24). Dogs with CSF results suggestive of disease other than stroke or with evidence of infectious disease were excluded. The available point of care ELISA test (Angio DetectTM IDEXX Europe B.V., Hoofed drop, The Netherlands) results were assessed, and dogs with a positive result were excluded from the analysis.
Anesthetic protocols were tailored to individual dogs by the attending anesthetist. MRI protocols and sequences varied between institutions, but all MRI examinations were completed with dogs under general anesthesia, using high-field-strength magnets: 1.5 Tesla (Hallmarq PetVet; Siemens Magnetom Sola; Canon Vantage Elan).
The MRI studies were reviewed by a European College of Veterinary Diagnostic Imaging board-certified veterinary radiologist (I.C.), and a third-year veterinary radiology resident (P.W.), on DICOM viewing software (OsiriX, Pixmeo, Switzerland). Reviewers were aware of the history, patient signalment, clinical, and neurological examination findings. Images were reviewed individually followed by consensus evaluation.
Data regarding treatment protocols were recorded for each patient. Survival was defined as the time from imaging diagnosis (MRI scan). Follow-up assessment was obtained from medical records where available.
Results
Sixty-three dogs met the inclusion criteria, 12 of which had lesions with T1w hyperintense signal without associated signal void on T2*w GE or SWI sequences (Figure 1). The median age was 7.5 years (range 5 months−11.5 years). Breeds included Greyhound (2), French Bulldog (2), Labrador Retriever (2), Cocker Spaniel (1), English Springer spaniel (1), Lurcher (1), West Highland White Terrier (1), Spanish Hound (1), and a Border Collie (1). Patients were female neutered (6), male neutered (3), female entire (2), and male entire (1).
Presenting clinical signs included acute or per-acute onset vestibular abnormalities (7/12), generalized seizures (4/12), collapse (2), unilateral blindness (2), and gait abnormalities (1). As detailed in Table 3, abnormalities documented on neurological examination by the attending neurologist included head tilt (7), proprioceptive deficits (6), head turn (3), circling (3), ataxia (3), tetraparesis (2 non-ambulatory, 1 ambulatory), hemiparesis (1), unilateral blindness (2), rotatory nystagmus (1), and vertical nystagmus (1). Documented cranial nerve abnormalities included absent or reduced menace (3 unilateral and 1 bilateral), absent pupillary light reflex (PLR) (1 unilateral), and absent vestibulocochlear (2) reflex, alongside left ventral strabismus, ptosis, and enophthalmos in one case. Hyperesthesia was not documented in any patient.
The exact time between the onset of clinical signs observed and the MRI assessment was recorded in 7/12 patients. All remaining (5/12) patients were scanned within 1 week of the onset of clinical signs. The mean time between the MRI scan and observed onset of clinical signs in this patient cohort was 3 days, with a range of 24 h to 21 days. As defined above, at the time of MRI scan, 9/12 patients had acute stroke, 2/12 had chronic stroke, and 1/12 had a subacute lesion. An example of the MRI sequence parameters used is provided in Table 2.
Upon MRI examination, all patients had a solitary lesion confined to the anatomical territory of a cerebral or cerebellar artery, and all lesions predominantly affected gray matter (12/12). These included 6/12 territorial lesions centered on territories of the middle cerebral (3), rostral cerebellar (2), and caudal cerebral arteries (1), alongside 6/12 lacunar infarcts centered on the irrigated region if the caudal perforating (3), lateral striate (2), and proximal perforating (1) arteries. Examples of such lesions are demonstrated in Figures 2–4, and a summary of imaging findings is detailed in Table 4.
All lesions (12/12) were homogeneously T2w and FLAIR hyperintense relative to both gray and white matter, and none had appreciable signal void on T2*w or SWI sequences. All lesions (12/12) were T1w hyperintense relative to both gray and white matter. When T1w signal hyperintensity was graded in comparison with the basal ganglia, 4/12 were described as mild, 6/12 moderate, and 2/12 severely T1w hyperintense. In terms of chronicity, the lesions with mild T1w hyperintensity were both acute (3) and subacute (1). Of the six (6/12) with a moderate T1w signal, 5/12 of these patients had acute lesions, and 1/12 had a chronic lesion. The severe T1w hyperintense signal noted in 2/12 was both acute (1) and chronic (1) in nature. In a large proportion of cases (6/12), the T1w hyperintense signal was distributed throughout the lesion, with a homogeneous (5/12) or heterogeneous pattern (1/12). Interestingly, in 6/12 cases, the observed T1w hyperintense signal had an almost linear, peripheral distribution, with a T1w hyperintense-isointense center. This was circumferential in three cases of lacunar infarction, located in the rostral thalamus, tegmentum, and caudate nucleus. In three cases of stroke of the middle cerebral artery, peripheral T1w hyperintensities were noted along the overlying cerebral cortices. In two of these cases, this most severely affected the outermost aspect of the cerebral cortex, in particular along the sylvian gyrus, marginal sulcus, and pseudosylvian fissure of the temporal and parietal lobes. In the third case, the peripheral T1w hyperintensity was most severe along the innermost cortex adjacent to the right pseudosylvian fissure, with a mild and heterogeneous T1w hyperintense signal throughout the remainder of the lesion.
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DWI sequences and apparent diffusion coefficient (ADC) maps were acquired in 7/12 cases. In 3/7 cases, lesions were hyperintense on DWI and hypointense on ADC, suggestive of restrictive diffusion. All of these lesions were acute in nature, corresponding with predominant cytotoxic edema seen in acute stages of infarction. Three (3/7) cases had lesions that were DWI hyperintense and ADC isointense relative to the contralateral gray matter, and these lesions were defined as acute (<1 week), subacute (8 days), and chronic (20 days) which may suggest an early stage of pseudonormalization, which is typically observed from 4 to 10 days of the ischemic event, secondary to cell lysis and subsequent facilitative diffusion (2). In one case, the infarct was ADC and DWI hyperintense, suggestive facilitative diffusion among cells due to a predominance of vasogenic edema. This corresponded with the chronicity of the lesion age (21 days).
All cases were assessed on T1w post-contrast, and 8/12 had a mild contrast enhancement. In 2/12, this was mild and heterogeneously distributed throughout, in 3/12, this was mild and homogeneously distributed throughout, and in 3/12, mild peripheral contrast enhancement was noted. The cases where peripheral contrast enhancement patterns were observed correlated with the observed distribution of the hyperintense signal on T1w pre-contrast images. Contrast enhancement was not evident in 4/12 cases.
The majority of lesions were well-demarcated (10/12). One was poorly defined due to extensive perilesional edema which extended into the surrounding white matter of the corona radiata and internal capsule. The second poorly defined lesion was centered on the caudate nucleus and, again, had a moderate amount of perilesional edema noted on FLAIR sequences. Mild perilesional edema was affecting four further lesions. The majority of cases had no associated mass effect (9/12). Three (3/12) cases exhibited mild mass attributable to the presence of perilesional edema, resulting in midline shift of the falx cerebri and mesencephalic aqueduct (2), and mild ventral compression of the left lateral ventricle (1). Parenchymal atrophy was not observed in any case.
Two cases had concomitant, likely chronic infarcts, appearing as small, discrete foci that were T2w hyperintense and T1w isointense to gray matter, with no contrast enhancement, perilesional edema, or signal void on T2*w GE or SWI sequences. One was in the territory of the left caudal perforating artery (left caudal thalamus) and the other in the right caudate nucleus. Neither of these concurrent lesions documented clinical signs attributable to their location, hence were presumed to be incidental findings at the time of image evaluation and at the time of image review.
Supportive treatment was provided to the majority of cases (7/12) which included aspirin (3) and clopidogrel (2), omeprazole (1), and anti-epileptic drugs, (1) while 5/12 had no treatment documented. The latter five cases showed initial neurological improvement while hospitalized, however, were subsequently lost to follow-up. The remaining 7/12 survived to discharge with clinical and neurological improvement documented in the medical records. Of these, further follow-up obtained in three cases showed resolution of neurological signs at 7 days (1), 1 month (1), and 1 year (1).
Discussion
This study documents the presence of T1w hyperintense signal in ischemic stroke without evidence of hemorrhage on T2*w GE or SWI sequences. This characteristic has been documented in human stroke patients (13–15, 28); however, to the authors' knowledge, this is the first report of this kind in clinical veterinary literature.
Twelve patients in this study had an intralesional T1w hyperintense signal compared to gray and white matter, and absence of signal void on T2*w GE or SWI sequences. When the distribution of the T1w hyperintense signal throughout the ischemic lesions was assessed, two clear patterns were observed; signal was either distributed throughout the entire lesion (6/12), or a more linear T1w hyperintensity was observed at the periphery of the lesion (6/12). This variation was observed in both lacunar (3/6) and territorial (3/6) lesions. The distribution of T1w hyperintense signal may reflect the inherent tissue susceptibility to hypoxia, or perfusion dynamics observed in ischemic stroke lesions (28–30). Consideration of the pathophysiology observed in ischemic stroke may help to explain the evolution of such signal change. Sequel to arterial occlusion, three separate regions of hypoperfused tissue are observed throughout the irrigated region, namely, the oligemic region, penumbra, and the infarct core (31). Oligemia refers to asymptomatic hypoperfused tissue that recovers without the need for reperfusion treatment and correlates with cerebral blood flow values that are reduced, but greater than the ischemic threshold of tissue (11). Ischemia refers to symptomatic hypoperfused tissue where cerebral blood flow is reduced below the cell's ischemic threshold (31). Within this, there is the infarct core of neural tissue that dies rapidly due to severe hypoperfusion, surrounded by the penumbra of salvageable hypoperfused tissue that has retained blood flow and metabolic function from collateral vasculature (31).
Less commonly reported sequelae of ischemic infarction include partial or incomplete infarction, selective neuronal necrosis (SNN), and cortical laminar necrosis (CLN) (17, 22, 28, 29, 32). These processes have demonstrated T1w hyperintense signal without corresponding hemorrhage in human stroke patients and experimental animal models, serving as potentially viable differentials for the hyperintense T1 signal observed in this patient cohort. All processes pertain to selective necrosis of neurons with preservation of less metabolically active cells, namely, endothelial cells, microglia, astroglia, and neurons, the death of which is conversely typical of tissue pannecrosis (13–16, 28). The terms, partial infarction and SNN, are frequently used interchangeably (28–30). Partial infarction is reported as a transient process in the acute stages of infarction and is seen in both transient ischemic attack or sequel to the development of pannecrosis (28, 33). Conversely, SNN is thought to persist into the chronic stages of infarction, potentially contributing to post-stroke cognitive decline observed in human neurodegenerative disorders such as vascular dementia (28, 32, 34). Both SNN and partial infarction have demonstrated similar patterns of delayed T1w hyperintensity within the affected tissue when studied in human patients and experimental animal models (13, 15, 17). Partial infarction and SNN have been identified histopathologically throughout the border zone of tissue infarction and throughout the penumbra on perfusion studies, which relates to the reduced cerebral perfusion throughout this region (35–39). However, SNN and partial infarction have also been observed throughout the entire lesion in some histopathological studies, resulting in a T1w hyperintense signal that is observed throughout the lesion entirety (28). Half (50%) of the patients in this study demonstrated a T1w hyperintensity throughout the entire lesion, whereas the remaining 50% had a peripherally distributed T1w hyperintense signal observed, meaning that when considering the conventional imaging features alone, both processes could account for the varied signal distribution observed.
The age of the lesions in our study also reflects temporal changes reported in studies of partial infarction and SNN. Histopathological studies in rats have demonstrated partial infarction to occur within 12 h following brief (10–25 min) occlusion of the middle cerebral artery (30), whereas experimental canine stroke models have observed T1w hypointense-isointense signal attributable to selective neuronal necrosis throughout the lesion within the first 3 days, a peripheral T1w hyperintense signal at 8 days, returning to a homogeneous T1w hypointense-isointense signal at 35 days (17). Similarly, T1w hyperintensities have been observed between 7 and 14 days in both humans and rats with neuronal necrosis secondary to acute cerebral infarction (14, 15). All patients in this cohort underwent MRI during the acute, subacute, or chronic stages of the ischemic event, with the mean age of the lesion being 3 days, and the range of lesion age being 1–21 days. Timings also correlated with the DWI/ADC signal intensity observed, where the majority of patients demonstrated DWI hyperintense and ADC hypointense signal, suggestive of restrictive diffusion typically seen within the first 4–10 days of an ischemic event (2, 5, 40). Given variation in timings reported for partial infarction, from 12 h, and selective neuronal necrosis, from 8 to 35 days, it is plausible that either process may account for the observed changes in our patient cohort.
Ostensibly, the presence of CLN could explain the peripheral T1w hyperintense signal observed in 3/6 cortical lesions of this study. Cortical laminar necrosis is a more specific subtype of infarction seen after global or focal ischemia that affects the cerebral cortex. It is a selective polioencephalomalacia occurring in response to transient or partial hypoxia or hypoglycemia, leading to necrosis of more metabolically active regions throughout cortical layers 3 and 5 (20, 34, 41, 42). T1-weighted (T1W) curvilinear hyperintense lesions affecting the gyral anatomy of the cerebral cortex are pathognomonic characteristics of cortical laminar necrosis on MRI imaging of human patients (22, 32). However, cortical laminar necrosis typically appears in the acute and subacute stages, frequently occurring at 8 days after the suspected hypoxic event, and being most pronounced at 1 month (32). These changes are somewhat more chronic than the majority of cortical lesions in our study, where indeed, MRI was performed within 24 h of the ischemic episode in two of the three cases of cerebral infarction in this patient cohort. Furthermore, cortical laminar necrosis is frequently limited to the gyral crests in cases of global ischemia, whereas in the three cases observed here, the linear T1w hyperintensity was observed along both sulcal and gyral margins overlying focal territorial regions of affected tissue (42). However, as cases of CLN have been observed in patients with regional ischemia, CLN cannot be completely excluded as a differential for cases affecting the cerebral cortex without histopathological analysis.
The exact pathophysiological mechanism for these overarching concepts of partial infarction and SNN is yet to be established (28). Histopathologically, these areas of selective neuronal death have demonstrated increased fat deposition, tissue calcification or mineralization, and increased protein accumulation resulting from glial responses and ultrastructural cellular alterations, all of which can attribute to T1 shortening (6, 18). Accumulation of minerals such as copper, manganese, and calcium within ischemic tissue can result from increased cellular oxidative stress and activation of various metabolic enzymes. These enzymes deposit paramagnetic mineral material throughout affected tissue, potentiating T1 shortening (14, 16). However, in line with our findings, the absence of mineral attenuation on CT studies of human patients and absence of associated signal void on SWI or T2*w MRI may oppose this theory of intralesional mineralization (13). Furthermore, histopathological assessment of human brains with T1w hyperintense ischemic lesions has failed to identify tissue mineralization, inferring that more than one pathophysiological mechanism may be responsible (15). Gemistocytic astrocytosis has been observed in T1w hyperintense lesions associated with SNN (16). Gemistocytic astrocytes, which usually appear in response to acute brain injury, have protein hydration layer which also results in T1 shortening (13). Post-ischemic ultrastructural changes in astrocyte cytoplasm, vacuolization, and proliferation of cellular organelles also increase the cellular protein content which can contribute to the hyperintense T1w tissue signal (16). Phagocytosis of damaged tissue by macrophages (microglia) and resultant intracellular lipid accumulation within microglia may also be responsible for the observed T1w hyperintensity due to increased fat content of the affected tissue (15).
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Further histopathological studies are warranted to confirm the presence of partial infarction or selective neuronal necrosis within the T1w hyperintense lesions observed. Furthermore, longitudinal prospective studies in clinical patients documenting temporal changes on MRI would be helpful to establish the evolution of these lesions and to provide further understanding of their prognostic value. Similarly, studies correlating these non-hemorrhagic T1w hyperintensities with perfusion-weighted imaging to investigate the flow dynamics within the affected region are warranted to further out understanding of the pathophysiological mechanisms involved.
This study is limited first by the small patient sample size. However, this condition is scarcely reported in human patients and is rarely seen in veterinary patients, meaning that cases with these changes are challenging to recruit (25, 26). Furthermore, follow-up MRI assessment is rarely performed in dogs, in particular if a positive response is observed clinically, as it is not ethically justifiable for such cases a second general anesthetic. This means that the temporal evolution of stroke in clinical studies is difficult to evaluate, and if such T1w hyperintensities are transient or delayed features, may not be present at the time of the MRI assessment. Nevertheless, future studies across a larger patient cohort are warranted to establish the temporal evolution of T1w hyperintense signal seen in non-ischemic stroke in canine patients. This study is also limited by its retrospective nature and multicenter design, meaning that study protocols cannot be unified, and in particular the strength of the MRI magnet and gradient coils is not uniform between centers. Furthermore, the clinical relevance of these lesions is difficult to ascertain as many patients in this cohort were lost to follow-up. Lastly, histopathological assessment was not available for any patient in this study, which is largely reflective of the inclusion criteria and nature of CVA, whereby none of the patients in our study were euthanized throughout the time of patient recruitment. Future studies across a larger patient cohort assessing perfusion parameters, clinical outcomes, and follow-up MRI assessment are warranted for further investigation.
Conclusion
Non-hemorrhagic T1w hyperintense signal observed in ischemic stroke has, to date, been rarely reported in canine patients. These lesions may be seen both within cortical territorial infarcts, or smaller lacunar infarcts throughout the non-cortical parenchyma, and can have either a homogeneous or peripheral distribution. Although the precise pathophysiology of this signal remains unknown, the presence of a T1w hyperintense signal in absence of signal void may raise suspicion of partial tissue infarction or selective neuronal necrosis, rather than early hemorrhagic transition in stroke cases.
Data availability statement
The datasets presented in this study can be found in online repositories. The names of the repository/repositories and accession number(s) can be found in the article/supplementary material.
Ethics statement
Ethical review and approval was not required for the animal study because this study is retrospective in nature, hence all procedures performed were for diagnostic or therapeutic purposes deemed necessary by the handling clinician at the time of presentation. Furthermore, consent was obtained from each owner for the use of the patients images and medical records in research studies upon admission of the patient. Written informed consent was obtained from the owners for the participation of their animals in this study.
Author contributions
IC conceived of the presented idea. PW and IC performed the image evaluation. PW wrote the manuscript. All authors contributed to the article and approved the submitted version.
Funding
Linnaeus Veterinary Limited supported the costs of the Open Access Publication Charges.
Conflict of interest
Authors PW, SB, and IC were employed by Linnaeus Veterinary Ltd.
The remaining authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest.
Publisher's note
All claims expressed in this article are solely those of the authors and do not necessarily represent those of their affiliated organizations, or those of the publisher, the editors and the reviewers. Any product that may be evaluated in this article, or claim that may be made by its manufacturer, is not guaranteed or endorsed by the publisher.
References
— Update: 13-03-2023 — cohaitungchi.com found an additional article Here Are the Most Important Things You Need to Know About Stimulating a Guy’s Prostate from the website www.cosmopolitan.com for the keyword how many strokes of his cock can he chandle.
Hey! The story you’re about to read was published prior to our April 2020 investigation on the G-spot. The truth is: It doesn’t exist. Learn more here.
For as much ink as the G-spot (or um, lack thereof) gets for people with vaginas, the prostate also gets trotted out as the penis-haver’s companion erogenous zone. It’s no secret that the prostate is a serious e-zone for those with penises, but whether or not they’ve fully explored it themselves is another matter. Just like its mysterious G-spot counterpart, the P-zone seems equally shrouded in conflicting advice on where it is, how to find it, and how to stimulate it most effectively for both of you. Here’s a beginner’s guide on how to stimulate someone’s prostate in a way that takes their pleasure to the next level, and in turn, make sex even better for both of you.
This sensitive, walnut-size gland is located within the body, behind the penis, and it contains tons of nerve endings, making it a perfect target for pleasure. That’s why some people refer to it as the “male G-spot” and still others as the “male P-spot.” In fact, some men are able to orgasm from prostate stimulation alone, although it is rare. It is most easily stimulated through the rectum and responds well to very gentle touch, whether from lubed-up fingers or from toys designed to be prostate massagers.
Since it can be more than a little intimidating to just casually dive right into butt play without having a game plan, there are a few things you should know about how to approach male G-spot stimulation as well as some solid and useful background on exactly what this gland is. Thankfully, Azaria Menezes, a sex and relationship coach, Tara Suwinyattichaiporn, a professor of sexual and relational communication at California State University, Fullerton, Fran Walfish, PsyD, a Beverly Hills–based family and relationship psychotherapist, and Lelo sexpert Laurie Mintz, PhD, author of Becoming Cliterate: Why Orgasm Equality Matters—and How to Get It, are here to explain everything you could possibly need to know about the prostate.
1. Always, always talk about it beforehand in a safe, judgment-free zone.
Just as you probably wouldn’t like a surprise finger up the bum, don’t do that to your partner either. Discuss what your partner is comfortable with beforehand, and everything you’ll try out before, says Menezes. This can also be a great time to debunk any stigmas your partner might have about exploring their prostate, or any fears about exploring prostate play, she says. “As this can sometimes be a vulnerable area to explore, be sure that you emphasize and create a safe, no-judgment zone for your partner to feel emotionally relaxed as well.”
2. Stay away from numbing agents.
If you’ve ever been curious about butt stuff, you’ve likely heard this advice before, but it bears repeating for you and your partner, as there’s a chance they haven’t heard it if they’ve otherwise mostly been on the giving end of anal play.
While desensitizing lubes and numbing agents might seem like a good idea at first, pain is your body’s way of letting you know to pause and go slower or re-assess things entirely, Menezes says. Plus, for your partner with the prostate, they’d probably want to experience all the sensations, whether they’re amazing (you are trying to stimulate an erogenous zone after all) or telling you to slow down a bit, Menezes adds.
3. Start small.
As exciting as it might be to set aside one day to tackle prostate play, you don’t wanna go from 0-60. Even if your partner is super gung-ho about the idea, it’s always better to start with something small, so the receiver can explore their pleasure in a non-intimidating way, says Menezes. Starting with your pinky finger or a smaller butt plug would be a better bet than going straight for a full-on, six or seven inch toy or dildo.
4. Rev up the foreplay beforehand.
In the same way foreplay can make intimidating acts like anal sex better and more pleasurable for you, the same should be done for your partner. Suwinyattichaiporn suggests experimenting with different oral sex techniques here, ranging from licking their scrotum like an ice cream cone, sucking on each testicle slowly, and massaging or rubbing their pubic area and inner thighs.
5. Offer to shave their testicles and or the area around their anus.
Sounds strange but bear with us. The prostate is in such a vulnerable place, and many people can feel a bit self conscious of their anus when it comes to hygiene. Of course, the key to this is in the offering and how you ask. Let them know it’s only if it would make them feel more comfortable from a receiving perspective and that you don’t mind either way. Can’t stress enough how you don’t want to pull a Big Ed here and just like, presumptuously demand they be shaved. Even though this isn’t necessarily a sexual act, Suwinyattichaiporn explains that this activity builds trust in the relationship. Not to mention, if it also makes them feel more comfy in the moment, that’s awesome too.
6. If you’re going to try milking their prostate, read up on exactly what to do beforehand so you have a game plan.
Milking a person’s prostate refers to the act of massaging their prostate to the point where the receiver ejaculates prostatic juices. It’s not called milking because semen looks like milk, which is what some (okay fine, me) people would think. For a more detailed play-by-play on exactly how to milk someone’s prostate, we’ve got tips from doctors and experts here for you. While “prostate play” is a general, vague-ish term, once you’ve got a pinky finger in there, you don’t want to freeze because you’re not actually sure on what to do once you’re in there.
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7. Use the “come hither” motion with your fingers to find it.
Mintz says that once your finger is about two inches in, press it forward against the wall of their perineum and try a “come here” motion with your fingers. Mintz adds: “You can also try moving your fingers in circles around the prostate or move your finger slowly back and forth, side to side.”
8. It feels like a walnut.
You’ll know you’ve found it when your finger pads reach something that feels like a walnut. Keep communication open, as your partner should also be able to tell you that they feel increased sensitivity when you touch it.
9. You may hear people talk about “milking” the prostate.
Giving a prostate massage for stimulation is sometimes referred to as “milking,” not because anything comes out but because you’re manipulating it with your hand, similar to how you’d manipulate the udder of a cow during the milking process.
10. It’s often referred to as the male G-spot.
Regardless of the fact that the existence of the female G-spot is still up for debate (researchers believe it’s actually just an extension of the clitoris), it’s still pretty impressive that the prostate has the same connotations as a one-stop-shop button for instantaneous orgasm. Walfish explains that the prostate contains many sensitive nerve endings that can provide a powerful orgasm. Mintz explains that in the book that popularized the G-spot for those with vaginas, the authors compared the clitoris to the penis and the G-spot to the prostate.
11. It’s not as far in as you’d think.
The prostate is about three-quarters of a finger length inside the anus, Walfish explains, and feels similar to a walnut.
12. Communication is key.
“Even if you’ve agreed to try anal sex, don’t just assume it’s going to happen this time,” Walfish says. “Request permission to board!” Active consent is not only sexy but also nonnegotiable.
13. Prep together.
It’s understandable that butt play might get messy, but if you want to cut down on that anxiety, Walfish says to try showering or bathing together with your partner, taking time to wash and lather each other’s genitals and anus. Not only is it super hot, but you can rest easy knowing you’ve both gotten clean in a nonjudgmental fashion.
14. Ease into it.
As with all sex, you don’t want it to feel too clinical. Walfish suggests easing into it, using a finger to gently massage the area at the opening of their anus or letting your tongue slide over the area while giving them oral sex. You can also use your hands to stroke it with your thumb while moving your fingers around the shaft.
15. You can stimulate it indirectly too!
As a good warm-up for direct prostate stimulation (or on its own), Mintz suggests using two fingers to massage their perineum (area between their scrotum and anus) from the outside as they reach climax.
16. Don’t underestimate the importance of lube.
Think about how painful it is to be (sorry) dry-fingered. While your vagina self-lubricates, your anus doesn’t. So lube is extra important with any butt play. Lelo’s personal moisturizer is a water-based lube that looks like a fancy bottle of cologne, so they truly have no excuse to throw it into some drawer to hide it, only to lose it forever. You’ll want to wet both their anus and your fingers.
17. Practice the golden rule of fingering.
Finger unto others as you would have them do unto you. This means cut and file your fingernails (no jagged edges fresh from the clippers!), wash your hands, and don’t jackhammer your fingers in and out—once you’re up there, you’re up there. It’s not about going in and out but more about massaging the gland once you’re in there (more on that later).
18. Relaxation is everything.
After massaging your partner’s perineum, spend several minutes massaging the outside of their anal opening. Mintz says that if you’ve been doing everything correctly, the sphincter should relax and open up. “Don’t insert farther than he is comfortable. If your finger meets resistance, stop there. You can call it a day and try again another time.”
19. Avoid sudden movements.
When you’re finished, pull your fingers out slowly. Sudden movements are not great with butt play, since the area can be sensitive. Nobody likes surprises!
20. Try using vibrators to stimulate their perineum and or prostate.
Look for a vibrator that’s curved to hit the prostate specifically. There’s no pressure to use it inside their butt the first go-around (just like with your sex toys, sometimes using it externally is all you really need), but if you want the most bang for your buck, you may as well invest in something that’s capable of that if you want to explore that down the line. The Lelo Loki features a bulbous tip perfect for prostate play, is rechargeable and waterproof, and has six different settings.
Shop Now Loki, $169, lelo.com
For those who want the latest in sex-toy tech, get the Loki Wave. It’s also specially designed for prostate stimulation, and the wand even does the “come hither” motion for you!
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21. You can also try stimulating their prostate at the same time as their penis.
No need to sign yourself up for penis and prostate stimulation right from the get-go—you’ll probably both need to concentrate on the task at hand. But once you’ve gotten comfortable with it, you can try adding other elements like oral sex, hand jobs, breast sex, and intercourse.
22. See if they like it better when they’re facing up or when they’re facing down.
Mintz says some people like it better one way or the other. Try it out both ways and compare notes! Is there one position that makes it more or less comfortable? Is there one movement you do that feels best? Communication makes everything better.
This article was originally published in 2008 and has been updated.
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— Update: 20-03-2023 — cohaitungchi.com found an additional article The 8 erogenous zones to hit for better orgasms—and how from the website www.womenshealthmag.com for the keyword how many strokes of his cock can he chandle.
Research from 2018 found that 50% of men surveyed cannot label where the vagina is on a picture of the female body. Wow.
The Eve Appeal polled 1,000 men to assess just how confused they were about the female body and potential gynaecological issues.
The charity said that these areas are still ‘shrouded in mystery’. So, time to clear a few things up…
First things first. Read our very extensive guide to the vagina parts, and then acquaint yourself and your partner with these key vulva-owner erogenous zones.
It’s not just where it’s also how that makes all the difference for mission orgasm.
Various types of touch – be it delicate caresses, firm pressure or vibration – feel different depending on which part of the body they’re applied to, according to a study published in The Journal of Sexual Medicine. In other words, a feather-light tickle may not even register in one particular spot but bold pressure applied on said area will have you en route to climax in seconds, says the study’s lead author and sexology researcher Dr Dany Cordeau.
(Note: while this article refers to sex between a woman or a person with a vagina, and a man or a person with a penis, there is obviously no reason why any gender pairing, with the right accessories, can’t have all learn a thing or two.)
Your erogenous parts: 8 sweet spots to know
1. The mouth
Even a peck is enough to ignite the brain’s passion centres (and bolster emotional bonding, says research in the Archives of Sexual Behavior).
Start off with soft kisses, using mostly lips, before escalating to the tongue.
2. The neck
This area has a high concentration of light-touch receptors, according to Cordeau, that go wild for gentle kisses and even a soft tickle of breath.
Encourage your partner to rub, suck or lightly scratch the back of your neck, just below your hairline, which is an especially erotic spot, says sexologist Carol Queen.
3. The nipples
Playing with your headlights is known to spark the same brain area that’s ignited when you masturbate, producing a similarly erotic sensation.
Light-to-medium pressure works well here, so “tell your man to suck on your nipple”, says sex and relationship expert Emily Morse. Your partner can also activate the nipples’ temperature-discerning nerves by first circling them with ice, then lightly drizzling them with warm wax from a candle (try soy-based which has a lower melting point and is less likely to burn the skin), says Queen.
4. The clitoris
Boasting 1,000 crowded nerve endings, it’s your most sensitive body part – so much so, you may not like immediate attention there if you haven’t been warmed up first.
Instead, get blood flowing by asking him to rub you tenderly on the thighs or the belly before zeroing in on the C-spot, says Queen.
Once you’re sufficiently turned on, medium pressure in a circular motion (using fingertips) or vibration (with a toy) at a fast speed are the best ways to fire up the clitoris, according to Cordeau’s findings.
5. The bum
Beyond squeezing and spanking, a lot of women enjoy some form of anal play, says LA sex therapist Amie Harwick, author of The New Sex Bible for Women. The anal nerves share a wall with your G-spot, which may explain why.
But sufficient arousal and lube are essential, says Morse. Tread slowly, with your partner first using his fingers to circle the opening. Okay with that? He can insert one finger, graduating to two.
6. The ears
They’re deemed an erogenous zone because of their neural tenderness, notes a study in the journal Plastic Surgical Nursing, so go for a bit of lobe-nibbling or sucking – a move that can feel especially good if you have piercings, says Queen.
Turns out the piercing puncture disrupts nerves’ pathways to the brain, making the area even more sensitive.
7. The vagina
The super-vulnerable skin on the outer edge responds to light touch, like stroking and gentle vibration, while the inner part prefers pressure, motion and fullness.
Stimulation inside also releases the hormone prolactin, which promotes a sense of sexual satisfaction.
Have your partner tease the opening of your vagina with one finger, then insert two lubricated digits inside you, curving them as he pushes in and out to increase fullness.
8. The areolae
The skin surrounding the nipples doesn’t have as many nerves as the bullseye itself, so subtle pinching can be more effective than a barely-there stroke. He can also squeeze, rub or cup your breasts to rev this zone.
“Have him put a finger on each side of your nipple to add more feel-good pressure,” says Queen.
Want to take things up a notch? Try introducing a vibrating toy to stimulate these zones. It’ll blow your mind.
Now you’ve learnt all about the erogenous spots, read about STI symptoms in women and PCOS symptoms.
