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Internist, Neurologist (brain, nervous system)
42 years of experience
Accepting new patients
Video profile


Education ?

Medical School Score Rankings
Johns Hopkins University (1970)
Top 25%

Awards & Distinctions ?

Castle Connolly America's Top Doctors® (2004 - 2008, 2010 - 2015)
Castle Connolly Top Doctors: New York Metro Area™ (1998 - 2008, 2010 - 2015)
Patients' Choice Award (2012 - 2013)
Compassionate Doctor Recognition (2013 - 2014)
Suny Downstate Medical Center College Of Medicine, Brooklyn, Ny (1977 - Present)
American Board of Psychiatry and Neurology
American Board of Internal Medicine

Affiliations ?

Dr. Kula is affiliated with 23 hospitals.

Hospital Affiliations



    Top 50%
  • Vassar Brothers Medical Center
    45 Reade Pl, Poughkeepsie, NY 12601
    Top 50%
    Top 50%
  • North Shore University Hospital
    300 Community Dr, Manhasset, NY 11030
    Top 50%
  • New York Methodist Hospital
    506 6th St, Brooklyn, NY 11215
  • Long Island Jewish Medical Center
    27005 76th Ave, New Hyde Park, NY 11040
  • North Shore Univ Hosp At Glen Cove
    101 Saint Andrews Ln, Glen Cove, NY 11542
  • North Shore Univ Hosp At Forest Hills
    10201 66th Rd, Forest Hills, NY 11375
  • Kings County Hospital Center
    451 Clarkson Ave, Brooklyn, NY 11203
  • Brooklyn University Hospital
    445 Lenox Rd, Brooklyn, NY 11203
  • North Shore University Hospital At Syosset
    221 Jericho Tpke, Syosset, NY 11791
  • North Shore Univ Hosp At Plainview
    888 Old Country Rd, Plainview, NY 11803
  • National Institutes of Health
  • New York College of Osteopathic Medicine
  • University Hospital
  • Long Island Jewish Medical Center-Schneider Children`s Hospital
  • V A Hospital - Brooklyn
  • Steven and Alexandra Cohen Childrens Med Ctr of NY
  • Suny Downstate Mc at Lich
  • Website
  • North Shore Univ at Manhasset
  • Www.Chiariinstitute.Com
  • Steven and Alexandra Cohen Children’s Medical Center of New York
    26901 76th Ave, New Hyde Park, NY 11040
  • Publications & Research

    Dr. Kula has contributed to 18 publications.
    Title Association of Chiari Malformation Type I and Tethered Cord Syndrome: Preliminary Results of Sectioning Filum Terminale.
    Date August 2009
    Journal Surgical Neurology

    The pathogenesis of CM-I is incompletely understood. We describe an association of CM-I and TCS that occurs in a subset of patients with normal size of the PCF.

    Title Surgical Management of Hydrocephalic Dementia in Paget's Disease of Bone: the 6-year Outcome of Ventriculo-peritoneal Shunting.
    Date July 2005
    Journal Clinical Neurology and Neurosurgery

    Paget's disease of bone is a chronic progressive skeletal disorder usually occurring in the long bones and skull of older adults and elderly persons. In the skull, softening of the skull base may lead to basilar impression and consequently obstruction of the cerebrospinal fluid through the basilar cisterns, resulting ventricular enlargement in association with gait difficulties, incontinence and dementia: a syndrome resembling normal pressure hydrocephalus. The optimal management of hydrocephalus associated with Paget's disease of the skull is not well documented and is still debated. We report a patient with hydrocephalic dementia linked to Paget's disease of the skull who showed marked sustained improvement in her neurological condition after ventriculo-peritoneal shunt insertion. We have now followed this patient for 6 years. Our experience supports the view that ventricular shunting is the procedure of choice for treating hydrocephalus linked to the Paget's disease of bone and is best carried out in the early stages of the illness.

    Title Peripheral Nervous System Complications of Sickle Cell Disease.
    Date January 2004
    Journal Annals of Neurology
    Title Visuoconstructive Deficit Following Infarction in the Right Basal Ganglia: a Case Report and Some Experimental Data.
    Date December 2003
    Journal Archives of Clinical Neuropsychology : the Official Journal of the National Academy of Neuropsychologists

    Visuospatial disorders are typically described as a consequence of right hemisphere, cortical lesions. We report the case of a female with visuoconstructive deficits with an infarct in the right basal ganglia, with no evidence of visual field defect, hemi-inattention, or sensory or motor loss. Using a process approach to obtain additional quantitative data, we showed that her visuoconstructive disorder could not be attributed to a defect in visual perception, per se. All other aspects of her neuropsychologic skills were normal. These findings provide additional support for the role of subcortical structures in spatially-related motor function and for the utility of applying experimental techniques to clarify the nature of deficits.

    Title Chronic Fatigue Syndrome: What Role Does the Autonomic Nervous System Play in the Pathophysiology of This Complex Illness?
    Date March 2003
    Journal Neuroimmunomodulation

    Chronic fatigue syndrome (CFS) is a serious health concern affecting over 800000 Americans of all ages, races and socioeconomic groups and both genders. The etiology and pathophysiology of CFS are unknown, yet studies have suggested an involvement of the autonomic nervous system (ANS). A symposium was organized in December 2000 to explore the possibility of an association between ANS dysfunction and CFS, with special emphasis on the interactions between ANS dysfunction and other abnormalities noted in the immune and endocrine systems of individuals with CFS. This paper represents the consensus of the panel of experts who participated in this meeting.

    Title Impairment of Slow Inactivation As a Common Mechanism for Periodic Paralysis in Diis4-s5.
    Date May 2002
    Journal Neurology

    BACKGROUND: Mutations in the human skeletal muscle sodium channels are associated with hyperKPP, hypoKPP, paramyotonia congenita, and potassium-aggravated myotonia. This article describes the clinical manifestations of a patient with hyperKPP carrying a mutation (L689I) occurring in the linker DIIS4-S5 and its functional expression in a mammalian system. OBJECTIVE: To correlate the clinical manifestations of hyperkalemic periodic paralysis (hyperKPP) with the functional expression of a sodium channel mutation. METHODS: The mutation was introduced into a mammalian expression vector and expressed in the human embryonic kidney 293 cells. The functional expression of the L689I and that of the wild-type channels was monitored using the whole cell voltage-clamp technique. RESULTS: There was no change in the kinetics of fast inactivation, and inactivation curves were indistinguishable from that of wild-type channels. However, the L689I mutation caused a hyperpolarizing shift in the voltage dependence of activation and the mutant channels showed an impaired slow inactivation process. In addition, the mutant channels have a larger persistent current at -40 mV where window current may occur. CONCLUSIONS: The L689I mutation has similar effects to the T704M mutation and causes hyperKPP in this family. Because both of these hyperKPP mutations cause episodic muscle weakness, and because patients harboring another mutation (I693T) also can have episodic weakness, it is hypothesized that mutations occurring in this region of the sodium channel may cause episodic weakness through an impaired slow inactivation process coupled with enhanced activation.

    Title Twenty-nine Years After Carbon Monoxide Intoxication.
    Date October 2001
    Journal Clinical Neurology and Neurosurgery

    Carbon monoxide (CO) is a worldwide environmental toxin and a leading cause of deliberate or accidental poisoning. There is an extensive literature devoted to the clinical features and treatment of those victims who have survived acute CO poisoning for a short length of time. The long-term sequelae of non-fatal poisoning have received scanty references, and the prospects for the long-lasting survivors of acute CO intoxication are less clear. Literature review uncovered reports of only three patients who were followed for a considerable period of time. We present a case of CO poisoning with progressive neurological and psychological deterioration that began 17 years after recovery from a severe, accidental CO asphyxia. The patient was examined in the neurology out patient clinic 29 years after the initial CO intoxication. We believe the unique status of this patient, her similarity to one other case in the literature and the circumstances allowing correlation of the clinical picture to the CO poisoning warrants emphasis.

    Title Chiari I Malformation Redefined: Clinical and Radiographic Findings for 364 Symptomatic Patients.
    Date June 1999
    Journal Neurosurgery

    OBJECTIVE: Chiari malformations are regarded as a pathological continuum of hindbrain maldevelopments characterized by downward herniation of the cerebellar tonsils. The Chiari I malformation (CMI) is defined as tonsillar herniation of at least 3 to 5 mm below the foramen magnum. Increased detection of CMI has emphasized the need for more information regarding the clinical features of the disorder. METHODS: We examined a prospective cohort of 364 symptomatic patients. All patients underwent magnetic resonance imaging of the head and spine, and some were evaluated using CINE-magnetic resonance imaging and other neurodiagnostic tests. For 50 patients and 50 age- and gender-matched control subjects, the volume of the posterior cranial fossa was calculated by the Cavalieri method. The families of 21 patients participated in a study of familial aggregation. RESULTS: There were 275 female and 89 male patients. The age of onset was 24.9+/-15.8 years (mean +/- standard deviation), and 89 patients (24%) cited trauma as the precipitating event. Common associated problems included syringomyelia (65%), scoliosis (42%), and basilar invagination (12%). Forty-three patients (12%) reported positive family histories of CMI or syringomyelia. Pedigrees for 21 families showed patterns consistent with autosomal dominant or recessive inheritance. The clinical syndrome of CMI was found to consist of the following: 1) headaches, 2) pseudotumor-like episodes, 3) a Meniere's disease-like syndrome, 4) lower cranial nerve signs, and 5) spinal cord disturbances in the absence of syringomyelia. The most consistent magnetic resonance imaging findings were obliteration of the retrocerebellar cerebrospinal fluid spaces (364 patients), tonsillar herniation of at least 5 mm (332 patients), and varying degrees of cranial base dysplasia. Volumetric calculations for the posterior cranial fossa revealed a significant reduction of total volume (mean, 13.4 ml) and a 40% reduction of cerebrospinal fluid volume (mean, 10.8 ml), with normal brain volume. CONCLUSION: These data support accumulating evidence that CMI is a disorder of the para-axial mesoderm that is characterized by underdevelopment of the posterior cranial fossa and overcrowding of the normally developed hindbrain. Tonsillar herniation of less than 5 mm does not exclude the diagnosis. Clinical manifestations of CMI seem to be related to cerebrospinal fluid disturbances (which are responsible for headaches, pseudotumor-like episodes, endolymphatic hydrops, syringomyelia, and hydrocephalus) and direct compression of nervous tissue. The demonstration of familial aggregation suggests a genetic component of transmission.

    Title Anxiety Disorders in a Neuromuscular Clinic.
    Date July 1993
    Journal The American Journal of Psychiatry

    Twenty patients with myasthenia gravis and 15 patients with polymyositis/dermatomyositis were assessed with a structured interview. Fifteen patients (43%) were diagnosed with an anxiety disorder. Significantly more myasthenic patients (40%) than polymyositis/dermatomyositis patients (7%) were diagnosed with panic disorder/agoraphobia. These findings suggest that the symptoms of myasthenia gravis may predispose vulnerable individuals to panic disorder/agoraphobia.

    Title Centronuclear Myopathy Heterogeneity: Distinction of Clinical Types by Myosin Isoform Patterns.
    Date February 1991
    Journal Neurology

    We studied muscles from 3 patients with centronuclear myopathy (CNM) by immunocytochemistry using myosin heavy chain (MHC)-specific monoclonal antibodies to determine whether subtypes of CNM express prenatal MHC and to assess if there is an arrest in development of these muscles. Muscle from a woman with childhood-onset CNM did not express prenatal MHC, yet this prenatal MHC was strongly expressed in the muscle fibers of 2 brothers with X-linked CNM. This finding represents the 1st immunocytochemical evidence of the expression of a prenatal myosin isoform in nonregenerating postnatal human muscle and suggests that the X-linked form of CNM differs from the other types because of a true arrest in maturation of the muscle.

    Title Inclusion Body Myositis.
    Date November 1990
    Journal Current Opinion in Rheumatology
    Title Detection of Human T-cell Lymphoma/leukemia Virus Type I Dna and Antigen in Spinal Fluid and Blood of Patients with Chronic Progressive Myelopathy.
    Date May 1988
    Journal The New England Journal of Medicine

    The presence of antibodies to human T-cell lymphoma/leukemia virus Type I (HTLV-I) has been associated with chronic progressive myelopathy. We attempted to isolate the virus from the blood and spinal fluid of patients with chronic progressive myelopathy and to define the clinical, radiologic, and electrophysiologic features of this disease. Ten of 13 patients from tropical countries and 2 of 8 from the United States had serum antibodies to HTLV-I. The virus was detected in cultures of peripheral-blood lymphocytes from three of seven patients by means of Southern blot hybridization. Using a sensitive in vitro enzymatic gene-amplification technique, we detected HTLV-I sequences in fresh peripheral-blood mononuclear cells of all of 11 patients tested who were positive for the antibody, and in cell cultures of the spinal fluid from 3 of the 11 tested. Magnetic resonance imaging of the cranium revealed periventricular lesions in the white matter of 3 of the 12 antibody-positive patients. Five of these patients had mild axonal sensorimotor polyneuropathy, and one had bilateral lumbar radiculopathy. Visual evoked potentials were abnormal in three seropositive patients, and brain-stem evoked responses were abnormal in two. The detection of the DNA and proteins of HTLV-I strengthens the proposition that this virus is involved in the pathogenesis of a subset of cases of chronic progressive myelopathy.

    Title Rhabdomyolysis in Leptospirosis (weil's Disease).
    Date October 1987
    Journal The Journal of Infectious Diseases
    Title Fiber Types in Normal and Neonatally Denervated Fast Muscles of the Rat: Immunocytochemical Study with an Antimyosin Monoclonal Antibody.
    Date October 1987
    Journal Experimental Neurology

    The differentiation of fiber types in normal and neonatally denervated gastrocnemius muscles of the rat was compared by myosin ATPase histochemistry and immunocytochemistry using a monoclonal antibody, HM-1.2. The specificity of HM-1.2 for the fast myosin heavy chain was determined by radioimmunoassay, immunoautoradiography, and indirect immunofluorescence techniques. In normal 1-month-old and adult rats, the type IIB (fast glycolytic) fibers of the gastrocnemius could be clearly divided into three subtypes by their graded immunofluorescence staining with the myosin heavy chain-specific monoclonal antibody. In the gastrocnemius muscle of the newborn rat, all fibers were negative with the monoclonal antibody. The transition from negative to three grades of immunoreactivity occurred 1 to 2 weeks postnatally. After neonatal denervation of the gastrocnemius muscle, however, uniformly positive monoclonal antibody immunofluorescence staining for the myosin heavy chain was observed without subtype differentiation. This study, thus, gave clear immunocytochemical evidence that the type IIB muscle fibers are heterogeneous with respect to their myosin isoform and that the expression of this heterogeneity is dependent on the normal developmental influence of motor innervation on the muscle fibers.

    Title I-cell Disease (mucolipidosis Ii). Differential Expression in Satellite Cells and Mature Muscle Fibers.
    Date April 1984
    Journal Journal of the Neurological Sciences

    A well documented case of I-cell disease is presented. Light- and electron-microscopic studies of muscle revealed marked accumulation of characteristic I-cell inclusions in satellite cells and only scattered autophagic vacuoles in muscle fibers. Correlation with previous tissue culture studies indicated an amelioration of structural abnormalities with differentiation from satellite cell to mature muscle fiber. Histochemically, the muscle demonstrated paucity of type I fibers without evidence of denervation thus suggesting a developmental disturbance in motor unit organization. Selective type I fiber dysfunction and reduced satellite cell regenerative capacity may be related factors in the neuromuscular disability of patients with I-cell disease.

    Title Alteration of Brain Stem Auditory Evoked Responses Following Cardio-respiratory Arrest and Resuscitation.
    Date October 1982
    Journal Electroencephalography and Clinical Neurophysiology

    BAERs were recorded in a patient who suffered spontaneous cardio-respiratory arrest after testing had begun. During the arrest the BAERs initially decreased in amplitude and then could not be recorded. After restoration of cardiac activity there was immediate recovery of waves I and II. Subsequent potentials also immediately reappeared but they did not recover their original peak latency values during the 50 min following resuscitation.

    Title Electrophysiologic and Histochemical Observations in Five Patients with Muscle Phosphorylase Deficiency (mpd).
    Date October 1978
    Journal Transactions of the American Neurological Association
    Title Scanning for Soft-tissue Amyloid.
    Date February 1977
    Journal Lancet

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