Pegah Kahaliardabili (Kahali), MD
Clinical Assistant Professor, Adult Neurology
Bio
Dr. Pegah Kahaliardabili (Kahali) is a board-certified neurologist and fellowship-trained movement disorders specialist at Stanford Health Care. She is also a clinical assistant professor in the Movement Disorders Division of the Department of Neurology and Neurological Sciences at Stanford University School of Medicine.
Dr. Kahali specializes in diagnosing and treating Parkinson’s disease and atypical parkinsonian syndromes, as well as hyperkinetic movement disorders such as tremor, dystonia, and chorea. She also cares for patients with ataxia and genetic movement disorders. Her procedural expertise includes deep brain stimulation (DBS), MR-guided focused ultrasound (MRgFUS), and intraoperative neurophysiology, including microelectrode recording. Dr. Kahali takes an individualized approach to treatment, considering each patient’s symptoms, goals, and overall health when developing a care plan.
Dr. Kahali’s research focuses on the neural mechanisms underlying motor and cognitive dysfunction in Parkinson’s disease and other movement disorders. Her work uses electrophysiological approaches, including EEG and intracranial recordings, to identify biomarkers of motor and cognitive function and to better understand their relationship to clinical outcomes. She is particularly interested in applying these biomarkers to developing more precise and individualized approaches to neuromodulation, including DBS. At Stanford, she collaborates on research investigating electrophysiological markers of cognitive vulnerability in Parkinson’s disease and their relationship to cognitive outcomes following DBS.
Dr. Kahali has published research in peer-reviewed journals including Proceedings of the National Academy of Sciences (PNAS), PLOS Computational Biology, and Anesthesia & Analgesia. Her research has been presented at national and international scientific meetings, including the Society for Neuroscience annual meeting and the Movement Disorder Society International Congress. She has also given invited clinical presentations on Parkinson’s disease, cognitive dysfunction, movement disorders, DBS, and neurophysiology.
Dr. Kahali is a member of the Movement Disorder Society (MDS) and the American Academy of Neurology (AAN).
Clinical Focus
- Neurology
- Movement Disorders
- Parkinson’s disease and atypical parkinsonian syndromes
- Hyperkinetic movement disorders (tremor, dystonia, chorea)
- Ataxia and genetic movement disorders
Honors & Awards
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Young Investigator Travel Award, Functional Neurosurgery Research Center, Iran
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Teaching Award, USC/LA General Medical Center (2023, 2024)
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Quality of Life Grant for Early Career Dialogues, MIT School of Science
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Golden Hammer, University of Southern California (USC)/Los Angeles (LA) General Medical Center
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Distinguished Medical Intern for Excellence in Medical Practice, Tehran University of Medical Sciences, Iran
Boards, Advisory Committees, Professional Organizations
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Member, MDS (2022 - Present)
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Member, AAN (2017 - Present)
Professional Education
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Board Certification: American Board of Psychiatry and Neurology, Neurology (2024)
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Residency: University of Southern CA Los Angeles Medical Center Neurology Residency (2024) CA
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Internship: Mount Sinai Health System Internal Medicine Residency Program (2021) NY
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Medical Education: Tehran University of Medical Sciences (2014) Iran
Current Research and Scholarly Interests
Electrophysiological biomarkers of motor and cognitive control, and precision neuromodulation in movement disorders.
All Publications
- From nodal- to network-centric, state-based neuromodulation for neuropsychiatric disorders Deep Brain Stimulation 2026
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Propofol disrupts alpha dynamics in functionally distinct thalamocortical networks during loss of consciousness.
Proceedings of the National Academy of Sciences of the United States of America
2023; 120 (11): e2207831120
Abstract
During propofol-induced general anesthesia, alpha rhythms measured using electroencephalography undergo a striking shift from posterior to anterior, termed anteriorization, where the ubiquitous waking alpha is lost and a frontal alpha emerges. The functional significance of alpha anteriorization and the precise brain regions contributing to the phenomenon are a mystery. While posterior alpha is thought to be generated by thalamocortical circuits connecting nuclei of the sensory thalamus with their cortical partners, the thalamic origins of the propofol-induced alpha remain poorly understood. Here, we used human intracranial recordings to identify regions in sensory cortices where propofol attenuates a coherent alpha network, distinct from those in the frontal cortex where it amplifies coherent alpha and beta activities. We then performed diffusion tractography between these identified regions and individual thalamic nuclei to show that the opposing dynamics of anteriorization occur within two distinct thalamocortical networks. We found that propofol disrupted a posterior alpha network structurally connected with nuclei in the sensory and sensory associational regions of the thalamus. At the same time, propofol induced a coherent alpha oscillation within prefrontal cortical areas that were connected with thalamic nuclei involved in cognition, such as the mediodorsal nucleus. The cortical and thalamic anatomy involved, as well as their known functional roles, suggests multiple means by which propofol dismantles sensory and cognitive processes to achieve loss of consciousness.
View details for DOI 10.1073/pnas.2207831120
View details for PubMedID 36897972
View details for PubMedCentralID PMC10089159
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A hidden Markov model reliably characterizes ketamine-induced spectral dynamics in macaque local field potentials and human electroencephalograms.
PLoS computational biology
2021; 17 (8): e1009280
Abstract
Ketamine is an NMDA receptor antagonist commonly used to maintain general anesthesia. At anesthetic doses, ketamine causes high power gamma (25-50 Hz) oscillations alternating with slow-delta (0.1-4 Hz) oscillations. These dynamics are readily observed in local field potentials (LFPs) of non-human primates (NHPs) and electroencephalogram (EEG) recordings from human subjects. However, a detailed statistical analysis of these dynamics has not been reported. We characterize ketamine's neural dynamics using a hidden Markov model (HMM). The HMM observations are sequences of spectral power in seven canonical frequency bands between 0 to 50 Hz, where power is averaged within each band and scaled between 0 and 1. We model the observations as realizations of multivariate beta probability distributions that depend on a discrete-valued latent state process whose state transitions obey Markov dynamics. Using an expectation-maximization algorithm, we fit this beta-HMM to LFP recordings from 2 NHPs, and separately, to EEG recordings from 9 human subjects who received anesthetic doses of ketamine. Our beta-HMM framework provides a useful tool for experimental data analysis. Together, the estimated beta-HMM parameters and optimal state trajectory revealed an alternating pattern of states characterized primarily by gamma and slow-delta activities. The mean duration of the gamma activity was 2.2s([1.7,2.8]s) and 1.2s([0.9,1.5]s) for the two NHPs, and 2.5s([1.7,3.6]s) for the human subjects. The mean duration of the slow-delta activity was 1.6s([1.2,2.0]s) and 1.0s([0.8,1.2]s) for the two NHPs, and 1.8s([1.3,2.4]s) for the human subjects. Our characterizations of the alternating gamma slow-delta activities revealed five sub-states that show regular sequential transitions. These quantitative insights can inform the development of rhythm-generating neuronal circuit models that give mechanistic insights into this phenomenon and how ketamine produces altered states of arousal.
View details for DOI 10.1371/journal.pcbi.1009280
View details for PubMedID 34407069
View details for PubMedCentralID PMC8405019
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Low Frontal Alpha Power Is Associated With the Propensity for Burst Suppression: An Electroencephalogram Phenotype for a "Vulnerable Brain".
Anesthesia and analgesia
2020; 131 (5): 1529-1539
Abstract
A number of recent studies have reported an association between intraoperative burst suppression and postoperative delirium. These studies suggest that anesthesia-induced burst suppression may be an indicator of underlying brain vulnerability. A prominent feature of electroencephalogram (EEG) under propofol and sevoflurane anesthesia is the frontal alpha oscillation. This frontal alpha oscillation is known to decline significantly during aging and is generated by prefrontal brain regions that are particularly prone to age-related neurodegeneration. Given that burst suppression and frontal alpha oscillations are both associated with brain vulnerability, we hypothesized that anesthesia-induced frontal alpha power could also be associated with burst suppression.We analyzed EEG data from a previously reported cohort in which 155 patients received propofol (n = 60) or sevoflurane (n = 95) as the primary anesthetic. We computed the EEG spectrum during stable anesthetic maintenance and identified whether or not burst suppression occurred during the anesthetic. We characterized the relationship between burst suppression and alpha power using logistic regression. We proposed 5 different models consisting of different combinations of potential contributing factors associated with burst suppression: (1) a Base Model consisting of alpha power; (2) an Extended Mechanistic Model consisting of alpha power, age, and drug dosing information; (3) a Clinical Confounding Factors Model consisting of alpha power, hypotension, and other confounds; (4) a Simplified Model consisting only of alpha power and propofol bolus administration; and (5) a Full Model consisting of all of these variables to control for as much confounding as possible.All models show a consistent significant association between alpha power and burst suppression while adjusting for different sets of covariates, all with consistent effect size estimates. Using the Simplified Model, we found that for each decibel decrease in alpha power, the odds of experiencing burst suppression increased by 1.33-fold.In this study, we show how a decrease in anesthesia-induced frontal alpha power is associated with an increased propensity for burst suppression, in a manner that captures individualized information above and beyond a patient's chronological age. Lower frontal alpha band power is strongly associated with higher propensity for burst suppression and, therefore, potentially higher risk of postoperative neurocognitive disorders. We hypothesize that low frontal alpha power and increased propensity for burst suppression together characterize a "vulnerable brain" phenotype under anesthesia that could be mechanistically linked to brain metabolism, cognition, and brain aging.
View details for DOI 10.1213/ANE.0000000000004781
View details for PubMedID 33079876
View details for PubMedCentralID PMC7553194
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Image Registration to Compensate for EPI Distortion in Patients with Brain Tumors: An Evaluation of Tract-Specific Effects.
Journal of neuroimaging : official journal of the American Society of Neuroimaging
2018; 28 (2): 173-182
Abstract
Diffusion magnetic resonance imaging (dMRI) provides preoperative maps of neurosurgical patients' white matter tracts, but these maps suffer from echo-planar imaging (EPI) distortions caused by magnetic field inhomogeneities. In clinical neurosurgical planning, these distortions are generally not corrected and thus contribute to the uncertainty of fiber tracking. Multiple image processing pipelines have been proposed for image-registration-based EPI distortion correction in healthy subjects. In this article, we perform the first comparison of such pipelines in neurosurgical patient data.Five pipelines were tested in a retrospective clinical dMRI dataset of 9 patients with brain tumors. Pipelines differed in the choice of fixed and moving images and the similarity metric for image registration. Distortions were measured in two important tracts for neurosurgery, the arcuate fasciculus and corticospinal tracts.Significant differences in distortion estimates were found across processing pipelines. The most successful pipeline used dMRI baseline and T2-weighted images as inputs for distortion correction. This pipeline gave the most consistent distortion estimates across image resolutions and brain hemispheres.Quantitative results of mean tract distortions on the order of 1-2 mm are in line with other recent studies, supporting the potential need for distortion correction in neurosurgical planning. Novel results include significantly higher distortion estimates in the tumor hemisphere and greater effect of image resolution choice on results in the tumor hemisphere. Overall, this study demonstrates possible pitfalls and indicates that care should be taken when implementing EPI distortion correction in clinical settings.
View details for DOI 10.1111/jon.12485
View details for PubMedID 29319208
View details for PubMedCentralID PMC5844838
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Automated white matter fiber tract identification in patients with brain tumors.
NeuroImage. Clinical
2017; 13: 138-153
Abstract
We propose a method for the automated identification of key white matter fiber tracts for neurosurgical planning, and we apply the method in a retrospective study of 18 consecutive neurosurgical patients with brain tumors. Our method is designed to be relatively robust to challenges in neurosurgical tractography, which include peritumoral edema, displacement, and mass effect caused by mass lesions. The proposed method has two parts. First, we learn a data-driven white matter parcellation or fiber cluster atlas using groupwise registration and spectral clustering of multi-fiber tractography from healthy controls. Key fiber tract clusters are identified in the atlas. Next, patient-specific fiber tracts are automatically identified using tractography-based registration to the atlas and spectral embedding of patient tractography. Results indicate good generalization of the data-driven atlas to patients: 80% of the 800 fiber clusters were identified in all 18 patients, and 94% of the 800 fiber clusters were found in 16 or more of the 18 patients. Automated subject-specific tract identification was evaluated by quantitative comparison to subject-specific motor and language functional MRI, focusing on the arcuate fasciculus (language) and corticospinal tracts (motor), which were identified in all patients. Results indicate good colocalization: 89 of 95, or 94%, of patient-specific language and motor activations were intersected by the corresponding identified tract. All patient-specific activations were within 3mm of the corresponding language or motor tract. Overall, our results indicate the potential of an automated method for identifying fiber tracts of interest for neurosurgical planning, even in patients with mass lesions.
View details for DOI 10.1016/j.nicl.2016.11.023
View details for PubMedID 27981029
View details for PubMedCentralID PMC5144756
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AUTOMATED CONNECTIVITY-BASED GROUPWISE CORTICAL ATLAS GENERATION: APPLICATION TO DATA OF NEUROSURGICAL PATIENTS WITH BRAIN TUMORS FOR CORTICAL PARCELLATION PREDICTION
IEEE. 2017: 774-777
View details for Web of Science ID 000414283200180
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Corticospinal tract modeling for neurosurgical planning by tracking through regions of peritumoral edema and crossing fibers using two-tensor unscented Kalman filter tractography.
International journal of computer assisted radiology and surgery
2016; 11 (8): 1475-86
Abstract
The aim of this study was to present a tractography algorithm using a two-tensor unscented Kalman filter (UKF) to improve the modeling of the corticospinal tract (CST) by tracking through regions of peritumoral edema and crossing fibers.Ten patients with brain tumors in the vicinity of motor cortex and evidence of significant peritumoral edema were retrospectively selected for the study. All patients underwent 3-T magnetic resonance imaging (MRI) including functional MRI (fMRI) and a diffusion-weighted data set with 31 directions. Fiber tracking was performed using both single-tensor streamline and two-tensor UKF tractography methods. A two-region-of-interest approach was used to delineate the CST. Results from the two tractography methods were compared visually and quantitatively. fMRI was applied to identify the functional fiber tracts.Single-tensor streamline tractography underestimated the extent of tracts running through the edematous areas and could only track the medial projections of the CST. In contrast, two-tensor UKF tractography tracked fanning projections of the CST despite peritumoral edema and crossing fibers. Based on visual inspection, the two-tensor UKF tractography delineated tracts that were closer to motor fMRI activations, and it was apparently more sensitive than single-tensor streamline tractography to define the tracts directed to the motor sites. The volume of the CST was significantly larger on two-tensor UKF than on single-tensor streamline tractography ([Formula: see text]).Two-tensor UKF tractography tracks a larger volume CST than single-tensor streamline tractography in the setting of peritumoral edema and crossing fibers in brain tumor patients.
View details for DOI 10.1007/s11548-015-1344-5
View details for PubMedID 26762104
View details for PubMedCentralID PMC4942409
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Common Genetic Variant in VIT Is Associated with Human Brain Asymmetry
FRONTIERS IN HUMAN NEUROSCIENCE
2016; 10
View details for DOI 10.3389/fnhum.2016.00236
View details for Web of Science ID 000376242300001
https://orcid.org/0000-0003-3959-4793