A 55-year-old African American woman presented with a chief complaint of dizziness to the otolaryngology clinic. She had been referred by a neurologist. The patient had a myocardial infarction (MI) 1 year previously, and since that time experienced constant, persistent dizziness with episodic bouts of “room-spinning” vertigo. She described her constant dizziness as “just dizzy all day, every day,” but said that positional changes, such as bending over or standing up too quickly, made it worse. The episodes of vertigo were preceded by a flulike prodrome consisting of diaphoresis, nausea, and numbness and tingling in her hands and feet. In 2 instances, she stated that she briefly lost consciousness. These episodes typically occurred twice per month, lasting from 5 minutes to a few hours, and were relieved by intravenous diazepam in the emergency department on at least 1 occasion. Meclizine was ineffective. The patient denied associated chest pain, palpitations, dyspnea, headaches, hearing loss, tinnitus, otalgia, aural pressure, or facial weakness. Findings from previous workups from a cardiologist and a neurologist were unremarkable, including normal orthostatic measurements, normal findings on Dix-Hallpike testing, and a normal magnetic resonance image of the brain. 

In addition to her MI and subsequent percutaneous coronary intervention with the placement of 2 stents, the patient's medical history was notable for multiple ear infections as a child and posttraumatic stress disorder (PTSD). Her medications included 81 mg of aspirin once daily, 40 mg of atorvastatin once daily, 75 mg of clopidogrel once daily, 5 mg of escitalopram once daily, 500 mg of ranolazine twice daily, and 20 mg of trospium twice daily. She lived alone and had to stop working because of her persistent symptoms. 

Physical examination revealed the patient to be alert and oriented, with normal mood and cognition. The HEENT (head, eyes, ears, nose, and throat) examination demonstrated that the head was normocephalic and atraumatic. Pupils were equal, round, and reactive to light. Eye movements were normal without evidence of nystagmus. External auditory canals were patent and clear of debris. Tympanic membranes were intact, mobile, and without middle effusion. Nose and throat examination findings were also normal. A neurologic examination revealed that cranial nerves II to XII were intact bilaterally. There was no evidence of dysarthria or short- or long-term memory deficits. Muscle tone was normal in all muscle groups, strength was +5/5 in the upper and lower extremities, and reflexes were +2/4 bilaterally. Finger-to-nose testing showed no abnormalities, no evidence of pronator drift was found, and gait was fluid and stable. On osteopathic structural examination, increased tension was noted throughout the cervical region, particularly in the upper cervical vertebrae. C3 was found to be extended, rotated, and sidebent left. The remainder of the examination findings were unremarkable. Audiogram and tympanometry results were normal. To more definitively rule out a vestibular origin, videonystagmography was used and yielded a normal result. Given these findings, our differential diagnosis included an underlying psychiatric cause (eg, PTSD, anxiety disorder, depression, or somatic symptom and related disorders), cardiac cause, or iatrogenic cause (eg, aspirin, escitalopram, ranolazine, or trospium). We informed the patient that an organic otologic cause was ruled out and suggested that she follow up with her primary care physician and to continue to follow up with her neurologist and cardiologist. 

This case demonstrates some of the challenges that face otolaryngologists and other physicians when a patient presents with dizziness. It may be difficult in some instances for physicians to elucidate the exact nature of the dizziness (eg, vertigo, presyncope, disequilibrium, nonspecific) when taking a history. In the current case, the patient depicted a chronic, constant dizziness that was difficult to describe and repeated vertiginous episodes with nausea, diaphoresis, and flulike symptoms. The patient's history of MI, timing of onset of her dizziness symptoms, and report of syncope associated with the vertiginous episodes also added to the complexity of the case. The clinical picture was even further complicated by the patient's psychiatric history and her use of multiple medications that could have caused or contributed to her dizziness symptoms. 

On further reflection and a review of the literature, multiple elements of the current case suggest an underlying psychiatric disorder. First, the patient described symptoms of chronic dizziness. Not only did the patient complain of repeated vertiginous episodes that occurred over the span of months, but also constant, unremitting dizziness that was difficult to describe and persisted for about a year. Dizziness that is both chronic and nonspecific in nature should alert a physician to a possible psychiatric cause.^1,8-10 Second, the patient had a history of PTSD managed with escitalopram. Studies suggest that PTSD has been associated with ill-defined somatic symptoms, such as unexplained dizziness.^10-13 A known history of a psychiatric disorder should provide an early clinical clue to the physician. Up to 28% of patients with dizziness have reported symptoms of an anxiety disorder,¹⁴ and 1 in 4 patients with dizziness may meet criteria for panic disorder.¹⁵ Additionally, patients with an anxious, introverted personality trait have been reported to be at increased risk for chronic subjective dizziness (CSD).¹⁶ Although our patient did not have a known history of an anxiety disorder, patients with PTSD exhibit high rates of psychiatric comorbidity. Anxiety disorders are 2 to 4 times more prevalent in patients with PTSD,¹⁷ and somatic symptom disorder is 90 times more likely in patients with PTSD.¹⁸ Also, the patient stated that her more severe dizziness episodes were only relieved with intravenous diazepam, a medication known to improve symptoms of anxiety.¹⁹ Thus, the complex and at times vague description of symptoms, chronic course, history of a psychiatric disorder, and relief of episodes with a benzodiazepine should raise a physician's suspicion that the patient's dizziness is caused, or at least in part affected, by a psychiatric disorder. 

Given the often complex nature of presentation and the notion that psychiatric disorders could be either a cause or consequence of dizziness, researchers have sought to better understand the relationship between chronic dizziness and psychiatric disorders. Ruckenstein and Staab¹⁰ attempted to more precisely define the term psychogenic dizziness, and they introduced the clinical entity chronic subjective dizziness, which, according to Holle et al,²⁰ has been renamed persistent postural-perceptual dizziness and will be included in the 11th revision of International Statistical Classification of Diseases and Related Health Problems. Patients with CSD present with a similar symptom complex involving a persistent (most days for >3 months) sensation of nonvertiginous dizziness that may include at least 1 of these vague descriptors: heavy headedness, lightheadedness, a feeling of imbalance, a feeling that the floor is moving, or a feeling of disassociation from one's environment. In addition, patients with CSD may exhibit chronic hypersensitivity to their own motion or the motion of objects in the environment, and their symptoms may be worsened by complex visual stimuli (eg, crowded places). 

Ruckenstein and Staab⁹ found that 93% of patients with CSD had a psychiatric disorder, particularly anxiety disorder, that significantly contributed to their symptoms. Of note, only one-third of these patients had a primary anxiety disorder and no history of vestibular disorder or another disease that could cause dizziness.^10,21 Another one-third of patients with CSD had no history of a psychiatric disorder but had a neurootologic illness (eg, benign paroxysmal positional vertigo) that precipitated the onset of anxiety (otogenic CSD). The final one-third had a history of an anxiety or other psychiatric disorder, experienced an acute otogenic event or other medical condition that triggered dizziness, and then developed a worsening of the preexisting psychiatric disorder that resulted in CSD symptoms (interactive CSD). The authors asserted that regardless of CSD subtype, symptoms persisted if the underlying psychiatric disorder was not addressed. Thus, in patients with CSD, managing the underlying psychiatric disorder may be critical to therapeutic success. 

Effective management of CSD or a psychogenic cause of dizziness seems to be multifactorial. Research suggests that patient education can be a key first step in the therapeutic process.^9,22 Physicians who suspect CSD or a psychogenic origin should discuss psychosocial issues with these patients and the ways in which psychiatric disorders and stress can cause or exacerbate chronic dizziness. For instance, a physician can initiate this conversation by focusing on the topic of stress: “In many patients, stress can also contribute to or worsen dizziness. How has stress affected your life recently?” These discussions can lay the foundation for successful treatment and, if necessary, psychiatric referral. Second, the mainstay of CSD management is pharmacotherapy with selective serotonin reuptake inhibitors (SSRIs). Studies indicate that these medications are effective in managing CSD.^23-25 Approximately 50% of patients given an SSRI had complete remission of symptoms, and 70% demonstrated a positive effect.^23-25 Physicians should recognize and counsel patients that SSRIs can cause an initial increase in anxiety symptoms and thus should initially be taken at low doses, with a slow titration. Of note, in the aforementioned study,¹⁰ patients with the interactive subtype of CSD did not respond as well to SSRIs. This finding appears relevant to the current case, as the patient may have had this form of CSD, given her history of PTSD and the onset of chronic dizziness after her MI. Furthermore, the patient had persistent symptoms despite taking 5 mg of escitalopram, although this dose may have been subtherapeutic. Other research indicates that psychotherapeutic techniques, such as cognitive behavioral therapy, may also benefit patients with CSD.^10,26,27 

A whole-person approach is emphasized in osteopathic philosophies, through which the union of body, mind, and spirit is recognized.²⁸ Given this principle, the apparent relationship between chronic dizziness and psychiatric disorders should not be surprising. A whole-person approach to patient care can help physicians recognize that patients with chronic dizziness, particularly CSD, are often frustrated.¹⁰ Often, these patients have seen several physicians and undergone multiple diagnostic tests and therapeutic trials for their symptoms, as exhibited in the current case. These patients may be disappointed by an absent diagnosis and ineffective prior treatments. Physicians in any specialty who possess a strong working knowledge of how psychiatric disorders can affect or cause chronic dizziness will be better equipped to help their patients. Furthermore, taking a whole-person approach to patients, gathering thorough psychosocial histories, and providing high-level compassion and respect for these patients can promote more effective clinical encounters and ultimately contribute to better outcomes.²⁸ The interrelationships between structure and function are also applicable to patients with chronic dizziness. As seen in the current case, the patient exhibited cervical dysfunction on physical examination. Research suggests that neck pain can be associated with psychiatric disorders.²⁹ Osteopathic manipulative treatment (OMT) could be an advantageous adjunctive therapy, as studies have indicated that OMT (eg, craniosacral techniques, cervical techniques) can improve anxiety, depression, autonomic nervous system function, and dizziness.^30-34 

The present case describes a patient whom we suspect meets the criteria for psychogenic CSD. However, the case is greatly limited by the fact that the patient was lost to follow-up. Our next step would have been to have a detailed discussion with the patient about her psychosocial history and recommend that she follow-up with a psychiatrist. Additionally, no OMT was applied . Thus, we were unable to assess whether a treatment approach consistent with a CSD diagnosis would be effective. 

We believe that our case demonstrates that physicians who are faced with a complex case of chronic dizziness, particularly primary care physicians, otolaryngologists, neurologists, cardiologists, and psychiatrists, should consider the presence of underlying psychiatric disorders. Future case studies should strive to discuss the impact of evidence-based treatment approaches for CSD. Although research into chronic dizziness and psychiatric disorders has greatly progressed, more studies are necessary to uncover the underlying physiologic mechanisms that mediate CSD. Finally, we advocate for heightened awareness of and education about factors contributing to chronic dizziness, particularly as persistent postural-perceptual dizziness is added to the 11th revision of International Statistical Classification of Diseases and Related Health Problems. 

The patient's complex and nonspecific symptoms, persistent course, history of PTSD, and relief with a benzodiazepine all suggest that a psychiatric disorder may have contributed to the chronic dizziness. Physicians, regardless of specialty, should be mindful that psychiatric conditions can be a relatively common source of or contributor to chronic dizziness. Moreover, physicians who are well versed in psychogenic factors and their relationship with chronic dizziness will not only be more adept at recognizing this cause but also be better able to effectively treat these patients. Like many situations in medicine, maintaining an osteopathic, whole-person approach that considers psychosocial factors can greatly benefit patients with chronic dizziness.