Angela N. Mark, M.D.

Angela N. Mark, M.D.

Angela N. Mark, M.D.

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Personal Bio

Treatment Philosophy

I believe in an evidence-based approach to diagnosing and treating neurologic disease, that is, if high quality evidence is available. Patient education regarding their condition and treatment options is also critical in reinforcing the patient’s ownership of their own health.

Personal Interests

I enjoy music, the fine arts and going to the theatre.

Conditions & Procedures


Abnormal Magnetic Resonance Imaging (MRI), Anosmia , Auras, 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, Dysphagia, Epilepsy/Seizure Disorder, Facet Pain, Facial Pain, Fibromyalgia, Gait Abnormailty, Gait Issues, General Neurology, General Weakness, Head Pain, Headache, Hypoglossal Nerve Disorder, Infantile Spasms, Low Back Pain (LBP), Migraine Headaches, Neck Pain, Nerve Conduction Velocity (NCV), Occupational Injury, Ocular Migraines, Pain in Limbs, Parasthesia, paresthesias, Seizures, Spastic Paraparesis, Spasticity, Spinal Stenosis, Syncope, Trigeminal Neuralgia, Twitch, Vertigo, Visual Auras

General Information




NorthShore Medical Group

Academic Rank

Clinical Assistant Professor



Board Certified

Clinical Neurophysiology, Neurology

Clinical Service

Education, Training & Fellowships

Medical School

Johns Hopkins University Schl of Med, 2005


St. Joseph Mercy - Ann Arbor, 2006


University of Michigan Medical Center


Rush University Medical Center



NorthShore Medical Group

1000 Central St.
Suite 880
Evanston, IL 60201
847.570.2570 847.570.2073 fax This location is wheelchair accessible.


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  • Improved understanding of cortical injury by incorporating measures of functional anatomy.

    Brain : a journal of neurology 2003 Jul

    Authors: Crafton KR,
    Volume of injury is often used to describe a brain insult. However, this approach assumes cortical equivalency and ignores the special importance that certain cortical regions have in the generation of behaviour. We hypothesized that incorporating knowledge of normal brain functional anatomy into the description of a motor cortex injury would provide an improved framework for understanding consequent behavioural effects. Anatomical scanning was performed in 21 patients with a chronic cortical stroke that involved the sensorimotor cortex. Functional MRI (fMRI) was used to generate separate average activation maps for four tasks including hand, shoulder and face motor tasks in 14 controls. For each task, group average maps for contralateral sensorimotor cortex activation were generated. Injury to these maps was measured by superimposing each patient's infarct. These measurements were then correlated with behavioural assessments. In bivariate analyses, injury to fMRI maps correlated with behavioural assessments more strongly than total infarct volume. For example, performance on the Purdue pegboard test by the stroke-affected hand correlated with the fraction of hand motor map injured (r = -0.79) more strongly than with infarct volume (r = -0.60). In multiple linear regression analyses, measures of functional map injury, but not infarct volume, remained as significant explanatory variables for behavioural assessments. Injury to >37% of the hand motor map was associated with total loss of hand motor function. Hand and shoulder motor maps showed considerable spatial overlap (63%) and similar behavioural consequences of injury to each map, while hand and face motor maps showed limited overlap (10.4%) and disparate behavioural consequences of injury to each map. Lesion effects support current models of broad, rather than focal, sensorimotor cortex somatotopic representation. In the current cross-sectional study, incorporating an understanding of normal tissue function into lesion measurement provided improved insights into the behavioural consequences of focal brain injury.
    PMID: 12805118 [PubMed - as supplied by publisher]
  • Motor cortex activation is preserved in patients with chronic hemiplegic stroke.

    Annals of neurology 2002 Nov

    Authors: Cramer SC,
    Many central nervous system conditions that cause weakness, including many strokes, injure corticospinal tract but leave motor cortex intact. Little is known about the functional properties of surviving cortical regions in this setting, in part because many studies have used probes reliant on the corticospinal tract. We hypothesized that many features of motor cortex function would be preserved when assessed independent of the stroke-affected corticospinal tract. Functional MRI was used to study 11 patients with chronic hemiplegia after unilateral stroke that spared regions of motor cortex. Activation in stroke-affected hemisphere was evaluated using 3 probes independent of affected corticospinal tract: passive finger movement, a hand-related visuomotor stimulus, and tapping by the nonstroke index finger. The site and magnitude of cortical activation were similar when comparing the stroke hemisphere to findings in 19 control subjects. Patients activated each of 8 cortical regions with similar frequency as compared to controls, generally with a smaller activation volume. In some cases, clinical measures correlated with the size or the site of stroke hemisphere activation. The results suggest that, despite stroke producing contralateral hemiplegia, surviving regions of motor cortex actively participate in the same proprioceptive, visuomotor, and bilateral movement control processes seen in control subjects.
    PMID: 12402258 [PubMed - as supplied by publisher]
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