Afif Hentati, M.D.

Afif Hentati, M.D.

Afif Hentati, M.D.

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Personal Bio

Treatment Philosophy

I treat patients as if they were part of my own family.

Personal Interests

I enjoy spending time with my family.

Conditions & Procedures


Abnormal Magnetic Resonance Imaging (MRI), Baclofen Pump, Complicated Migraines, Demylinating Disease, Devic Disease, Dizziness, Facial Pain, Gait Abnormailty, Gait Issues, General Neurology, General Weakness, Head Pain, Headache, Hereditary Spastic Paraplegia, Migraine Headaches, Multiple Sclerosis (MS), Neck Pain, Optic Neuritis, Pain in Limbs, paresthesias, Spastic Paraparesis, Spasticity, Syncope, Transverse Myelitis, Trigeminal Neuralgia, Twitch, Vertigo

General Information




NorthShore Medical Group


Neurology, Multiple Sclerosis

Academic Rank

Clinical Assistant Professor


Arabic, English, French

Board Certified


Clinical Service

Education, Training & Fellowships

Medical School

Faculté de médecine de Sfax, 1984


University Hospitals of Sfax, 1986


University Hospitals in Tunisia, 1990
Northwestern Feinberg School of Medicine, 2001


McGaw Medical Center of Northwestern University, 1998



NorthShore Medical Group

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

NorthShore Medical Group

2180 Pfingsten Rd.
Suite 2000
Glenview, IL 60026
847.570.2570 847.570.2073 fax This location is wheelchair accessible.


Commercial Plans
  • Aetna Choice POS (Open Access) and POS II (Open Access)
  • Aetna Elect Choice EPO and EPO Open Access
  • Aetna Health Network Options
  • Aetna HMO (including Open Access)
  • Aetna Managed Choice (Open Access)
  • Aetna Managed Choice POS
  • Aetna Open Access Aetna Select (Aetna HealthFund)
  • Aetna Open Access Elect Choice EPO (Aetna HealthFund)
  • Aetna Open Access Managed Choice POS (Aetna HealthFund)
  • Aetna Open Choice PPO
  • Aetna Open Choice PPO (Aetna HealthFund)
  • Aetna Premier Care Network
  • Aetna QPOS
  • Aetna Select
  • Aetna Select (Open Access)
  • Beechstreet PPO Network
  • Blue Cross Blue Shield - PPO Products
    Not Contracted Blue Cross Blue Shield Blue Choice PPO
  • Blue Cross Blue Shield Blue Advantage
    Verify PCP Participation
  • Blue Cross Blue Shield HMOI
  • Cigna HMO
  • Cigna LocalPlus
  • Cigna Open Access Plus (OAP)
  • Cigna Open Access Plus with CareLink (OAPC)
  • Cigna POS
  • Cigna PPO
  • Cofinity PPO (an Aetna Company)
  • Coventry Health Care Elect Choice EPO
  • Coventry Health Care First Health PPO
  • Galaxy Health PPO Network
  • Great West PPO/POS
  • Healthcare's Finest Network (HFN)
  • Humana - All Commercial Plans (including Choice Care)
  • Humana - NorthShore Complete Care
  • Humana/ChoiceCare Network PPO
  • Medicare
  • Multiplan and PHCS PPO Network (Including PHCS Savility)
  • NorthShore Employee Network
  • Preferred Plan PPO
  • Three Rivers Provider PPO Network (TRPN)
  • Tricare
  • Unicare
  • United Healthcare - All Commercial Plans
    Not Contracted United Healthcare Core
    Not Contracted United Healthcare Navigate
Exchange Plans
  • Not Contracted Aetna
  • Blue Cross Blue Shield - PPO Products
    Not Contracted Blue Cross Blue Shield Blue Choice PPO
  • Blue Cross Blue Shield Blue Precision
    Verify PCP Participation
  • Not Contracted Coventry
  • Humana National
  • Land of Lincoln - All Products
  • Not Contracted United Healthcare Compass
  • Illinois Department of Public Aid (IDPA)
  • Illinicare ICP
  • Community Care Partners
Medicare Advantage Plans
  • Aetna Medicare (SM) Plan (HMO/Open Access HMO)
  • Aetna Medicare (SM) Plan (PPO)
  • Blue Cross Blue Shield Medicare Advantage PPO Plan
  • Cigna-HealthSpring Advantage HMO
  • Cigna-HealthSpring Premier HMO-POS
  • Cigna-HealthSpring Primary HMO
  • Humana Gold Plus HMO
  • Humana Gold Plus PFFS
  • HumanaChoice PPO
  • United Healthcare - All Medicare Plans
Medicare Medicaid Alignment Initiative (MMAI) Plans
  • Blue Cross Blue Shield Community
  • HealthSpring
  • Humana
  • Illinicare Health Plan
  • Meridian Complete


  • Live cell imaging of the nascent inactive X chromosome during the early differentiation process of naive ES cells towards epiblast stem cells.

    PloS one 2014

    Authors: Guyochin A,
    Random X-chromosome inactivation ensures dosage compensation in mammals through the transcriptional silencing of one of the two X chromosomes present in each female cell. Silencing is initiated in the differentiating epiblast of the mouse female embryos through coating of the nascent inactive X chromosome by the non-coding RNA Xist, which subsequently recruits the Polycomb Complex PRC2 leading to histone H3-K27 methylation. Here we examined in mouse ES cells the early steps of the transition from naive ES cells towards epiblast stem cells as a model for inducing X chromosome inactivation in vitro. We show that these conditions efficiently induce random XCI. Importantly, in a transient phase of this differentiation pathway, both X chromosomes are coated with Xist RNA in up to 15% of the XX cells. In an attempt to determine the dynamics of this process, we designed a strategy aimed at visualizing the nascent inactive X-chromosome in live cells. We generated transgenic female XX ES cells expressing the PRC2 component Ezh2 fused to the fluorescent protein Venus. The fluorescent fusion protein was expressed at sub-physiological levels and located in nuclei of ES cells. Upon differentiation of ES cell towards epiblast stem cell fate, Venus-fluorescent territories appearing in interphase nuclei were identified as nascent inactive X chromosomes by their association with Xist RNA. Imaging of Ezh2-Venus for up to 24 hours during the differentiation process showed survival of some cells with two fluorescent domains and a surprising dynamics of the fluorescent territories across cell division and in the course of the differentiation process. Our data reveal a strategy for visualizing the nascent inactive X chromosome and suggests the possibility for a large plasticity of the nascent inactive X chromosome.
    PMID: 25546018 [PubMed - as supplied by publisher]
  • VZV encephalitis that developed in an immunized patient during fingolimod therapy.

    Neurology 2015 Jan 6

    Authors: Michel S,
    Spontaneous regression of an epithelial thymic tumour has been reported but seems extremely rare. Its mechanism is unknown.
    We report two cases of epithelial thymic tumour, either histologically proven or highly suspected on imaging, that regressed spontaneously (partially in one patient and totally in the other).
    Spontaneous regression of an epithelial thymic tumour is very rare but this possibility could lead to clinical and radiological monitoring rather than surgery in selected patients.
    PMID: 25416038 [PubMed - as supplied by publisher]
  • Thoracoscopic partial thymectomy for untraceable mediastinal parathyroid adenomas.

    Interactive cardiovascular and thoracic surgery 2011 Nov

    Authors: Hentati A,
    Despite accurate preoperative imaging, ectopic mediastinal parathyroid adenomas can be difficult to find via a thoracic approach. Considering that - in most cases - these adenomas are intrathymic, it can be advisable to directly perform a partial thymectomy. We present the cases of three patients who were successfully cured using a thoracoscopic partial thymectomy.
    PMID: 21873366 [PubMed - as supplied by publisher]
  • Sequence alterations within CYP7B1 implicate defective cholesterol homeostasis in motor-neuron degeneration.

    American journal of human genetics 2008 Feb

    Authors: Tsaousidou MK,
    The hereditary spastic paraplegias (HSPs) are a genetically and clinically heterogeneous group of upper-motor-neuron degenerative diseases characterized by selective axonal loss in the corticospinal tracts and dorsal columns. Although numerous mechanisms involving defective subcellular transportation, mitochondrial malfunction, and increased oxidative stress have been proposed, the pathogenic basis underlying the neuronal loss is unknown. We have performed linkage analysis to refine the extent of the SPG5 disease locus and conducted sequence analysis of the genes located within this region. This identified sequence alterations in the cytochrome P450-7B1 (CYP7B1) associated with this pure form of HSP. In the liver, CYP7B1 offers an alternative pathway for cholesterol degradation and also provides the primary metabolic route for the modification of dehydroepiandrosterone neurosteroids in the brain. These findings provide the first direct evidence of a pivotal role of altered cholesterol metabolism in the pathogenesis of motor-neuron degenerative disease and identify a potential for therapeutic intervention in this form of HSP.
    PMID: 18252231 [PubMed - as supplied by publisher]
  • Meta-analysis of age at onset in spastin-associated hereditary spastic paraplegia provides no evidence for a correlation with mutational class.

    Journal of medical genetics 2003 Sep

    Authors: Yang Y,
    Amyotrophic lateral sclerosis (ALS) and primary lateral sclerosis (PLS) are neurodegenerative conditions that affect large motor neurons of the central nervous system. We have identified a familial juvenile PLS (JPLS) locus overlapping the previously identified ALS2 locus on chromosome 2q33. We report two deletion mutations in a new gene that are found both in individuals with ALS2 and those with JPLS, indicating that these conditions have a common genetic origin. The predicted sequence of the protein (alsin) may indicate a mechanism for motor-neuron degeneration, as it may include several cell-signaling motifs with known functions, including three associated with guanine-nucleotide exchange factors for GTPases (GEFs).
    PMID: 12960222 [PubMed - as supplied by publisher]
  • Novel mutations in spastin gene and absence of correlation with age at onset of symptoms.

    Neurology 2000 Nov 14

    Authors: Hentati A,
    Autosomal dominant hereditary spastic paraplegia is genetically heterogeneous, with at least five loci identified by linkage analysis. Recently, mutations in spastin were identified in SPG4, the most common locus for dominant hereditary spastic paraplegia that was previously mapped to chromosome 2p22. We identified five novel mutations in the spastin gene in five families with SPG4 mutations from North America and Tunisia and showed the absence of correlation between the predicted mutant spastin protein and age at onset of symptoms.
    PMID: 11087788 [PubMed - as supplied by publisher]
  • Linkage of a commoner form of recessive amyotrophic lateral sclerosis to chromosome 15q15-q22 markers.

    Neurogenetics 1998 Dec

    Authors: Hentati A,
    Autosomal recessive familial amyotrophic lateral sclerosis (RFALS) is a rare form of ALS that usually presents at an early age with slow progression of symptoms. RFALS is clinically and genetically heterogeneous and the locus of RFALS type 3 was mapped to 2q33 (ALS2) in a single family. We now report linkage of a more-common form of RFALS to chromosome 15q15-q22 markers (ALS5) and show further genetic locus heterogeneity in RFALS. ALS5 is the locus for most families with RFALS and appears to be present in both North African and European populations.
    PMID: 9933301 [PubMed - as supplied by publisher]
  • Familial amyotrophic lateral sclerosis.

    Journal of neural transmission. Supplementum 1997

    Authors: Siddique T,
    Amyotrophic lateral sclerosis is sporadic in ninety percent of cases and familial (FALS) in ten percent. Both forms of FALS whether transmitted as an autosomal dominant (DFALS) or as an autosomal recessive (RFALS) trait is genetically heterogeneous. The locus for one form of RFALS maps to chromosome 2q33. Fifteen percent of DFALS families have mutations in the gene for Cu, Zn superoxide dismutase (SOD1) gene which is coded on chromosome 21. These mutations result in decreased SOD1 activity and shortened half-life of the protein in most instances. Transgenic mice overexpressing mutated SOD1 protein develop an ALS-like disease which suggests that the degeneration of motor neurons in DFALS is caused by the gain of a novel toxic function by mutated SOD1 rather than by the decrease of SOD1 activity. Possible mechanisms of the novel neurotoxic function of mutated SOD1 are discussed.
    PMID: 9266431 [PubMed - as supplied by publisher]

In the News

Feb 2014

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