Education & Certifications


  • FRCP, University of Alberta, Adult Neurology Residency Program (2024)
  • MD, Northern Ontario School of Medicine (2018)
  • H. BHSc, University of Calgary, Health Sciences- Biomedical Sciences (2014)

All Publications


  • Mon frere. CMAJ : Canadian Medical Association journal = journal de l'Association medicale canadienne Purdy, K. 2021; 193 (47): E1828-E1829

    View details for DOI 10.1503/cmaj.210648-f

    View details for PubMedID 34844947

  • My brother. CMAJ : Canadian Medical Association journal = journal de l'Association medicale canadienne Purdy, K. 2021; 193 (36): E1433-E1434

    View details for DOI 10.1503/cmaj.210648

    View details for PubMedID 34518347

  • The Clinical Conundrum of Managing Ischemic Stroke in Patients with Immune Thrombocytopenia. The Canadian journal of neurological sciences. Le journal canadien des sciences neurologiques Alrohimi, A., Purdy, K., Alqarni, M., Alotaibi, G., Blevins, G., Butcher, K., Rempel, J., Wu, C., Sun, H. L., Khan, K. 2021; 48 (1): 38-46

    Abstract

    Guidelines are lacking for management of acute ischemic stroke and stroke prevention in patients with immune thrombocytopenia (ITP). Our aim is to highlight the dilemma inherent in managing patients with both significant bleeding and thrombotic risk factors. In this review, we present two patients with history of ITP who presented with acute ischemic stroke and received tissue plasminogen activator (tPA) and endovascular thrombectomy (EVT), a rare management strategy in this patient population. In addition, we identified 27 case reports of ischemic stroke in patients with ITP; none of them received tPA or EVT. Furthermore, there are 92 patients with significant thrombocytopenia with no available data regarding the cause of thrombocytopenia, who were acutely treated with tPA or EVT. Conclusive evidence cannot be determined based on these limited number of cases. Future multicenter prospective cohort studies in patients with ITP are needed to provide better evidence-based treatment plans. At present, treatment of acute ischemic stroke in patients with ITP requires close collaboration between hematology and vascular neurology experts to find a balance between the benefit and risk of hemorrhagic complications.

    View details for DOI 10.1017/cjn.2020.138

    View details for PubMedID 32646527

  • Diabetes and the Nervous System Aminoff's Neurology and General Medicine Purdy, K., Zochodne, D. W. Academic Press. 2021; 6: 303-316
  • The neurology residents of COVID-19. Neurology Purdy, K. 2020; 95 (11): 495

    View details for DOI 10.1212/WNL.0000000000010582

    View details for PubMedID 32764100

  • Can osmotic demyelination syndrome be a complication of liver failure? eNeurologicalSci Purdy, K., Anderson, D., Camicioli, R., Khadaroo, R. G. 2020; 18: 100223

    Abstract

    This case demonstrates that osmotic demyelination syndrome (ODS) can occur in absence of hyponatremia in patients with fulminant liver failure and markedly high bilirubin levels. Extremely high bilirubin levels, such as >900 μmol/L in the case presented here, may lead to blood brain barrier dysfunction by disrupting blood vessel endothelial cell function as well as increase the release of inflammatory cytokines. As demonstrated in the case here, even small fluctuations in electrolytes may make the brain increasingly more vulnerable to ODS. Clinicians should keep ODS high on their differential even in eunatremic patients with liver failure who have decreased levels of consciousness or coma.

    View details for DOI 10.1016/j.ensci.2020.100223

    View details for PubMedID 32055718

    View details for PubMedCentralID PMC7005432

  • Canadian Federation of Medical Students (CFMS) response to: The unmatched by Dr. Amit Persad. Canadian medical education journal Purdy, K., Silverberg, S. 2018; 9 (2): e93-e94

    View details for PubMedID 30018690

    View details for PubMedCentralID PMC6044303

  • Caspase-6 is a Dispensable Enabler of Adult Mammalian Axonal Degeneration. Neuroscience Woo, V., Cheng, C., Duraikannu, A., Chandrasekhar, A., Purdy, K., Martinez, J. A., Zochodne, D. W. 2018; 371: 242-253

    Abstract

    The progress of axonal degeneration (AxD) following injury or insult impacts both recovery from axonal transection and protection of axons from diverse insults, or axonopathy. Here we provide evidence that increases in capase-6 (Casp6) expression and action contribute to the progression of AxD. The expression of Casp6 protein and mRNA in distal branches of sensory axons undergoing AxD was confirmed. We developed and utilized a new model of axonopathy in live mice by serially visualizing the viability of cutaneous axons in the ear pinna that expressed an axonal YFP transgene, in response to capasaicin-induced AxD. Both specific pharmacological inhibition of caspase-6 and local knockdown offered early but subtle and mild attenuation of axonopathy. To evaluate an axon autonomous role of Casp6, we examined axon integrity following transection ex vivo, and analyzed the serial morphological fragmentation of neurofilament expression as a structural index of AxD. Adding a specific Casp6 inhibitor to the preparation delayed neurofilament fragmentation. Intact motor axons of Casp6 null mice had normal electrophysiological properties but, as tested serially during AxD, there was attenuated loss of excitability. Following transection, morphological features of AxD were evident in both wild type and Casp6-/- mice but the latter had evidence of slowed progression. Taken together, our findings suggest a subtle but dispensable enabling role of local Casp6 expression in axons undergoing AxD. Serial analysis of cutaneous ear pinna axons in live mice provides a useful and novel model of axonal integrity.

    View details for DOI 10.1016/j.neuroscience.2017.11.052

    View details for PubMedID 29229552

  • Unmatched Canadian medical graduates. CMAJ : Canadian Medical Association journal = journal de l'Association medicale canadienne Silverberg, S. L., Purdy, K. M. 2018; 190 (4): E118

    View details for DOI 10.1503/cmaj.68737

    View details for PubMedID 29378874

    View details for PubMedCentralID PMC5790563

  • A BRCA1-Dependent DNA Damage Response in the Regenerating Adult Peripheral Nerve Milieu. Molecular neurobiology Krishnan, A., Purdy, K., Chandrasekhar, A., Martinez, J., Cheng, C., Zochodne, D. W. 2018; 55 (5): 4051-4067

    Abstract

    It is not generally appreciated that DNA repair machinery has a critical role in the remodeling of neurons that adopt a regenerative phenotype. We identified that breast cancer 1 (BRCA1)-dependent DNA activity, previously well known to repair cancer cells, is active in adult peripheral neurons and Schwann cells during their injury and regeneration response. Temporary or partial loss of BRCA1 or blockade of its intraneuronal nuclear entry impaired outgrowth in neurons in vitro and impacted nerve regeneration and functional recovery in vivo. We found that distal axonal injury triggered a BRCA1-dependent DNA damage response (DDR) signal in neuronal soma. BRCA1 also supported an enabling transcriptional program of injured neurons and supporting Schwann cells. Our findings indicate that BRCA1 offers prominent functional roles in neurons and glial cells including key support for their physical and molecular integrity. Since BRCA1 mutations are common in humans, this function of BRCA1 in peripheral neurons and their glial partners warrants attention.

    View details for DOI 10.1007/s12035-017-0574-7

    View details for PubMedID 28585187

  • Enhancing adult nerve regeneration through the knockdown of retinoblastoma protein. Nature communications Christie, K. J., Krishnan, A., Martinez, J. A., Purdy, K., Singh, B., Eaton, S., Zochodne, D. 2014; 5: 3670

    Abstract

    Tumour suppressor pathways may offer novel targets capable of altering the plasticity of post-mitotic adult neurons. Here we describe a role for the retinoblastoma (Rb) protein, widely expressed in adult sensory neurons and their axons, during regeneration. In adult sensory neurons, Rb short interfering RNA (siRNA) knockdown or Rb1 deletion in vitro enhances neurite outgrowth and branching. Plasticity is achieved in part through upregulation of neuronal PPARυ; its antagonism inhibits Rb siRNA plasticity, whereas a PPARυ agonist increases growth. In an in vivo regenerative paradigm following complete peripheral nerve trunk transection, direct delivery of Rb siRNA prompts increased outgrowth of axons from proximal stumps and entrains Schwann cells to accompany them for greater distances. Similarly, Rb siRNA delivery following a nerve crush improves behavioural indices of motor and sensory recovery in mice. The overall findings indicate that inhibition of tumour suppressor molecules has a role to play in promoting adult neuron regeneration.

    View details for DOI 10.1038/ncomms4670

    View details for PubMedID 24752312

    View details for PubMedCentralID PMC5028199