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

Conditions

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

Gender

Male

Affiliation

NorthShore Medical Group

Expertise

Neurology, Multiple Sclerosis

Academic Rank

Clinical Assistant Professor

Languages

Arabic, English, French

Board Certified

Neurology

Clinical Service

Education, Training & Fellowships

Medical School

Faculté de médecine de Sfax, 1984

Internship

University Hospitals of Sfax, 1986

Residency

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

Fellowship

McGaw Medical Center of Northwestern University, 1998

Locations

A

NorthShore Medical Group

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

NorthShore Medical Group

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

Insurance

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)
  • 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
Medicaid
  • Community Care Partners
  • Illinicare ICP
  • Illinois Department of Public Aid (IDPA)
Medicare Advantage Plans
  • Aetna Medicare (SM) Plan (HMO/Open Access HMO)
  • Aetna Medicare (SM) Plan (PPO)
  • Blue Cross Blue Shield Medicare Advantage PPO Plan
    Effective 1/1/2015
  • 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

Publications

  • [Spontaneous regression of epithelial thymic tumours].

    Revue des maladies respiratoires 2012 May

    Authors: Michel S,
    Abstract
    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: 22682601 [PubMed - as supplied by publisher]
  • Thoracoscopic partial thymectomy for untraceable mediastinal parathyroid adenomas.

    Interactive cardiovascular and thoracic surgery 2011 Nov

    Authors: Hentati A,
    Abstract
    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,
    Abstract
    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,
    Abstract
    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,
    Abstract
    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,
    Abstract
    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,
    Abstract
    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]
  • A novel mutation in the sterol 27-hydroxylase gene of a Pakistani family with autosomal recessive cerebrotendinous xanthomatosis.

    Neurology 1997 Jan

    Authors: Ahmed MS,
    Abstract
    Cerebrotendinous xanthomatosis (CTX) is a rare autosomal recessive disorder of lipid storage with prominent neurologic features. The disease is associated with mutations in CYP27, which encodes mitochondrial sterol 27-hydroxylase, an enzyme that catalyzes the oxidation of sterol intermediates during bile acid synthesis. The loss of this enzyme results in accumulation of cholestanol in the nervous system and other tissues. Six different mutations have been previously described in CTX. We analyzed a Pakistani family, which included four affected individuals with clinical characteristics of CTX, for mutations in CYP27. The exons of CYP27 in the family DNA were amplified by polymerase chain reaction (PCR) and analyzed for mutations by band shifts (single stranded conformational polymorphism [SSCP]) and DNA sequencing. The PCR product for exon 4 showed an SSCP change in this family. The DNA of affected individuals showed an abnormal mobility pattern interpreted as homozygous for the mutation. One non-affected sibling was homozygous for the normal migrating pattern, whereas the parents and another non-affected sibling were heterozygous. The sequence of exon 4 of affected individuals showed a substitution of C to T in codon 237, thus substituting arginine to a stop codon. This mutation would terminate the translation, which may result in a protein half the size of the wild type rendering it practically inactive.
    PMID: 9008528 [PubMed - as supplied by publisher]
  • Molecular genetic basis of familial ALS.

    Neurology 1996 Oct

    Authors: Siddique T,
    Abstract
    Familial amytrophic lateral sclerosis (FALS) is transmitted in a mendelian fashion as an autosomal dominant (DFALS) or an autosomal recessive (RFALS) trait. Both DFALS and RFALS are genetically heterogeneous. Fifteen percent of DFALS families have mutations in the gene for Cu, Zn superoxide dismutase (SOD1) which is coded on chromosome 21. The locus for one form of RFALS maps to chromosome 2q33. Forty-six mutations in the SOD1 gene have been reported in DFALS families. 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. Several possible mechanisms of the novel neurotoxic function of mutated SOD1 are discussed.
    PMID: 8858048 [PubMed - as supplied by publisher]

In the News

Feb 2014

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