Irene A. Semenov, D.O.

Irene A. Semenov, D.O.

Irene A. Semenov, D.O.

Log into NorthShoreConnect


Personal Bio

Treatment Philosophy

My treatment approach is to focus on the whole person rather than a disease process. It emphasizes a strong and supportive doctor-patient relationship. My goals are to provide all of my patients with a compassionate and comprehensive care.

Personal Interests

I like music, running, traveling and cooking.

Conditions & Procedures


Abnormal Magnetic Resonance Imaging (MRI), Back Pain, Benign Paroxysmal Positional Vertigo (BPPV), Cerebral Palsy (CP) ( ages 18+ years), Cervicogenic Headaches, Chiari Malformation, Cluster Headache, Complicated Migraines, Degenerative Spine Disease, Dizziness, Dysarthria, Facial Pain, Gait Abnormailty, Gait Issues, General Neurology, General Weakness, Head Pain, Headache, Hypoglossal Nerve Disorder, Low Back Pain (LBP), Migraine Headaches, Neck Pain, Nerve Conduction Velocity (NCV), Occupational Injury, Ocular Migraines, Pain in Limbs, Parasthesia, paresthesias, Spastic Paraparesis, Spinal Stenosis, Syncope, Trigeminal Neuralgia, Twitch, Vertigo, Visual Auras

General Information




NorthShore Medical Group

Academic Rank

Senior Clinician Educator


English, Russian

Board Certified

Clinical Neurophysiology, Headache Medicine, Neurology

Clinical Service

Education, Training & Fellowships

Medical School

Midwestern University's Chicago College of Osteopathic Medicine, 2001


Lutheran General Hospital, 2002


McGaw Medical Center of Northwestern University, 2005


McGaw Medical Center of Northwestern University, 2006



NorthShore Medical Group

2180 Pfingsten Rd.
Suite 2000
Glenview, IL 60026
847.570.2570 847.657.5708 fax Get Directions This location is wheelchair accessible.

NorthShore Medical Group

9650 Gross Point Rd.
Suite 3900
Skokie, IL 60076
847.570.2570 847.657.5708 fax Get Directions This location is wheelchair accessible.

NorthShore Medical Group

757 Park Ave. West
Suite 2850
Highland Park, IL 60035
847.570.2570 847.657.5708 fax Get Directions This location is wheelchair accessible.



  • Migraine headaches.

    Disease-a-month : DM 2015 Jun

    Authors: Semenov IA
    TTH are very common in general population and may be under diagnosed. They are more common in patients suffering from migraine headaches. In general underlying psychiatric conditions, such as anxiety and depression, are prevalent in TTH sufferers. For acute therapy NSAIDs are the main treatment option. Tricyclic antidepressant, SSRI, and cognitive behavioral therapy have been proven to be effective for prophylactic purposes.
    PMID: 25911064 [PubMed - as supplied by publisher]
  • The relation of brain ouabain-like compounds and idiopathic intracranial hypertension.

    Headache 2006 Sep

    Authors: Borsody M, Semenov I, Carroll K, Kessler A, Dubow J, Olson E, Stern J, Barion A, Hammond C, Van Stavern G, Raizer J, White R, Leenen F
    To determine the relationship between levels of ouabain-like compounds (OLC) in the cerebrospinal fluid (CSF) and the occurence of idiopathic intracranial hypertension (IIH).
    OLC are naturally occurring inhibitors of the sodium-potassium ATPase that are found in the CSF of mammals. Since the production of CSF is dependent upon sodium-potassium ATPase activity, and since there is evidence that the increased intracranial pressure found in the condition of IIH may be the result of increased CSF production, we hypothesized that the level of endogenous OLC would be reduced in the CSF of patients with IIH.
    CSF samples were obtained from n = 7 patients with IIH and n = 31 patients with neurological disorders other than IIH ("control" patients) who had lumbar puncture as part of their routine evaluation or treatment. The concentration of OLC in the CSF samples was measured using an established ELISA.
    Patients with IIH exhibited a concentration of OLC in the CSF of 0.11 +/- 0.03 ng/mL. In comparison, the concentration of OLC in CSF samples from non-IIH control patients was 0.12 +/- 0.01 ng/mL. These values were not statistically different when compared with a t-test (P= 0.31). However, the concentration of OLC did negatively correlate to the opening pressure on lumbar puncture, but only in the IIH group (r=-0.80, P= .03). Furthermore, IIH patients who were newly diagnosed or who were unsuccessfully treated (n = 5 of 7 IIH patients) exhibited OLC concentrations of 0.06 +/- 0.1 ng/mL, which is nearly lower than that of the control group (P= .06).
    The average concentration of OLC in IIH patients (treated and untreated) is unlikely to be distinguishable from that in non-IIH control patients with other neurological conditions. However, the concentration of OLC may be inversely related to the intracranial pressure in patients with IIH, and it may prove to be lower in the subgroup of untreated and unsuccessfully treated IIH patients.
    PMID: 16942469 [PubMed - as supplied by publisher]
  • Focal neurological injury caused by West Nile virus infection may occur independent of patient age and premorbid health.

    Journal of the neurological sciences 2005 Jul 15

    Authors: Bhangoo S, Chua R, Hammond C, Kimmel Z, Semenov I, Videnovic A, Kessler J, Borsody M
    Limited evidence suggests that focal neurological injury (e.g., acute flaccid paralysis) caused by infection with the West Nile virus (WNV) is more common in older patients. We re-evaluate this association in a series of patients who were infected with the WNV during the 2002 epidemic.
    We performed a retrospective chart review of 34 patients who were hospitalized for treatment of serologically confirmed WNV infection. Measurements included the patient's demographic characteristics, baseline medical diagnoses, the occurrence of symptoms and exam findings, the results of various diagnostic tests, and the patient's clinical outcome.
    Patients infected with the WNV who developed focal neurological injury were found to be comparable to patients who did not develop focal neurological injury both in terms of patient age and the number of medical conditions the patient had prior to infection. This is in contrast to WNV-infected patients who developed an encephalitis-like clinical course, or who died or were institutionalized after their hospitalization; such patients tended to be older and-in cases with a poor outcome-have more medical conditions prior to WNV infection.
    In our patient group, focal neurological injury caused by WNV infection was not related to advanced patient age or to the number of medical conditions the patient had prior to infection. Our findings bring into question commonly held views about the development of focal neurological injury caused by WNV infection, and they raise concerns about the management of future WNV epidemics and the testing and use of potential antiviral treatments against this infection.
    PMID: 15958267 [PubMed - as supplied by publisher]