We report the case of a 46-year-old right-handed man who came to his district hospital with a right hemiplegia.
A brain CT scan showed a hematoma in the left hemisphere affecting the striated nucleus and the internal capsule.
The administration of intravenous contrast ruled out active bleeding, as well as structural abnormalities of the iliac crest or other arteriovenous malformations that could justify the bleeding.
However, hypoplasia of the left vertebral artery was detected.
He was diagnosed with arterial hypertension, for which he received the appropriate pharmacological treatment, and once stabilized he was referred to our rehabilitation service.
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The patient was classified as having neuropsychiatric assessment because his speech was strikingly enveloped and he showed an excessive deficit in his rehabilitation program and evolution.
Before the first interview with the patient, we had the opportunity to talk to his brother.
After belonging to the hospital, the patient came to the floor to collect some of the patient's personal data, and found a house practically full of books, DVDs, utensils, etc.
There was a narrow passage connecting the bedroom with the kitchen and bathroom.
In a more detailed examination, he observed that his brother had 3 or 4 copies of the same books.
He also said he had a lot of clothes, but of the same type (for example, the same type and color of pants or shirts...) and about 20 pairs of identical shoes.
Many toys he had preserved from his childhood and found themselves in perfect condition.
Though defeated, the floor was extremely cold.
Through what his brother said, we knew that the patient was born from a normal delivery and that he had normal psychomotor development in early childhood.
His brother remembered that at age 4 he was an "anxious" child who received "some type of medication" for a few days.
The patient used to take the toys of his brothers but did not provide his.
He came to school centers of some prestige obtaining good academic results, although with great effort.
Apparently during school time, he was excluded by his classmates, who made him "peculiar".
He completed university studies of law and, although it was published, it took 11 years to complete this degree of five.
He never worked as a train.
He stayed at home helping in different tasks.
When he took care of his grandfather, he was his caregiver and the same later with his parents, until he died.
His brother described him as "organized, scrupulous, prevented and perfectionist."
She said she used to take long showers and that she was very peculiar when she kept things, she had to do it in a specific way.
She had also observed tics that included the nose and neck, and that the patient had "from time to time" a tick tic.
He had not known a sentimental couple.
We then present the patient, whose appearance was slightly discouraged, although he was euthymic and with adequate affection.
He had a tic on his right arm, moving as if to replace his watch.
His speech was fluid and spontaneous, normal in the course, but extremely overactive and with Galician accent (from Galicia, northern Spain).
No symptoms were observed in the psychotic sphere.
When exploring the content of thought, he explained that he lived "a simple and flat life".
He paid attention to his grandmother and her parents, one after the other, and therefore justified not having exercised the lawyer.
She said she didn't think she had any problems before her CVA.
The fact that he had spoken with a Galician accent was certainly unexpected, since he had never visited that region, nor had family members or natural friends there.
She was reassessed with her brother 4 days later.
He admitted having about 20,000 books, 2,000 CDs, and more than 2,000 DVDs on his floor.
He said he used to buy them very cheap, and that if he saw one who liked him especially he used to buy three or four copies to be able to regulate his relatives and friends by Christmas or per birthday.
He referred to accumulating behavior as a "financial strategy" to make them pay at a reasonable price.
The same referred to the other articles found on the floor.
At no time did he perceive his situation as a problem, giving different but detailed justifications to explain his behavior.
Sensory-persistent alterations.
In the cognitive examination, the patient scored 30/30 in the MMSE and 92/100 in the ACEve (1) (Spanish version of the Addenbrooke's Cognitive Examination; (2)), with a worse verbal score (226/287).
Having explained 3/3 refranes was able to complete the Luria test with some effort.
A diagnosis of obsessive-compulsive disorder with chronic tics and accumulation was made, as well as foreign accent syndrome.
A psychopharmacological treatment based on sertraline was established, with progressive increase up to a daily dose of 150 mg, achieving a good evolution.
The discourse no longer turned out to be missive, although it maintained the Galician accent.
He continued without being aware of his illness, insisting that his conduct was a "good strategy", although he agreed not to buy more articles.
Follow-up consultation was scheduled after 4 months (6 months after stroke).
He had remained stable psychopathologically.
No tics were observed, and the Galician accent - although still present - was barely perceptible.
In the cognitive exploration, scores were 30/30 in the MMSE and 95/100 in the ACEve, having lost points in anterograde memory (27/28) and verbal fluency (6/7 for categories and 4/7 for categories).
Although she still did not accept OCD or accumulating behavior, she accepted treatment and follow-up.
He lived with a family member, and although he had not yet ordered his house, he had agreed with his brother to begin doing so after a more complete physical recovery.
After one year of stroke few changes were observed.
The foreign accent tics remained absent.
He continued living with a relative and focused his efforts on "physical recovery", so he had not had time to order his floor, although he agreed to focus on it after recovering.
The adherence to the pharmacological treatment was good and went regularly to the consultation of his general doctor, since he did not want to join the psychiatry service.
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Obsessive-compulsive disorder:
Obsessivecompulsive disorder (OCD) has a lifetime prevalence of 2-3 % (3).
It is characterized by the presence of obsessives and impulses.
Observing remains can be understood as thoughts, images or intrusive and unwanted impulses the subject recognizes as his own, despite having a disturbing and disturbing content.
Contamination, verification and inflicting harm to oneself and others are frequent ideas.
The subject, at least initially, does oppose resistance to these intrusive experiences, although he/she may face them over time.
On the other hand, compulses are defined as behaviors or acts mentalizing and ritualistic, which carry out an attempt to reduce anxiety generated by obscure cable.
These symptoms are distressing and chronically disabling (4.5).
A longitudinal study with 40-year follow-up showed that although most patients show some improvement over time, they usually present symptoms chronically (6).
The diverse subjective experiences that precede repetitions (icts or with impulses) are known there as "phenomena" and described (4) as "generalized repetitive behaviors" or preceding, focal sensations that are unpleasant,
Subsequent works have redefined this term, adding the need to perform additive behaviors until they feel that everything is "how it should be" or "perfect" (of the Englishman "just right"), knowing then as "perfect".
Other authors have proposed terms such as "body and mental sensations" (7); "impossible premonitory", "non-perfection" or "incomplete" to describe these phenomena.
With the objective of reaching a consensus for the definition of these experiences, the Miguel advocate team for maintaining the term "sensory phenomena" (8).
OCD is a clinically heterogeneous disorder.
Attempts to classify the disorder based on its clinical characteristics, often in mutually exclusive subgroups, have followed two different approaches: categorical or dimensional.
Factor analyses of different symptoms have supported the existence of four dimensional factors or phenotypic expressions of OCD: aggressive/comprogressive, obsessive sexual accumulation, factor II (pieness, factor III) and religious contamination (factor III).
These dimensions can overlap in their clinical presentation, coexisting in any patient, and show clinical stability over time (9-11).
Although the male-female ratio is 1:1, gender differences have been found both in the symptomatology and in the course of this disorder.
In men there are more antecedents of perinatal suffering, an earlier age of onset, more probability of not having been married, and a higher frequency of sexual obsessions I, precision and symmetry, as well as ritual factor.
Women, on the other hand, showed a higher age of onset of OCD, were more likely to be married at diagnosis, were less likely to be infected with OCD, 13 were more likely to suffer from bipolar disorder, 12 were obsessive.
Further research has focused on the study of familial aggregation of OCD.
Segregation segregation analysis results implying "dominant genetic effects" for dimensional factors I and II and "receptive genetic effects" for dimension factors III and IV (7).
The different symptomatic factor dimensions of OCD seem to be associated with different neuroanatomical pathways within the orbitofrontal-striate-thalamic circuit.
Thus, the "comprobation" (dimensional factor I) is associated with the activation of putamen/globo pale, thalamus and dorsal cortical areas, bilateral prefrontal and dimensional venipuncture (factor IV).
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Ict and OCD disorder:
Tics are movements, gestures or gestures that typically mimic fragments of normal behaviors.
Paroxysmal and short-term effects can also occur in clusters.
They range from simple and abrupt movements to objective behaviors.
Likewise, verbal or phonic tics can oscillate between a simple carraspeo to coprolalia in the most severe cases (15).
OCD with tics has its own clinical characteristics when compared to OCD without tics.
They usually appear at an earlier age (15.16), predominate in male patients (although some authors have not found these differences between genders) (17), they are associated with a family history of tics-specific disorder, have a neurochemical basis.
Individuals with a chronic tic disorder scored higher in the dimensional factors of aggressiveness/comprobation (I) and symmetry/order (II) preceded by simultaneous cognitions (1518).
An abnormal pattern of cortical excitability (21) has also been described.
Although the association OCD and tics is characteristic of another condition, Tourette Syndrome (TS), this pattern has also been observed in patients with OCD and chronic motor or verbal tics (22) who do not have (ST)
This differentiated phenotype of OCD, with a higher family burden, seems to be related to alterations in chromosome 9p, which condition a different genotype and allele frequencies of the allele A of the serotonergic receptor 5-HT2A (7.23).
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Psychiatric comorbidity:
There is a well-recognized prevalence of psychiatric disorders comorbid to OCD.
The scientific literature shows that 15% of patients initially diagnosed with OCD were subsequently diagnosed with schizophrenia or bipolar disorder.
These tend to have an earlier age of onset and a worse prognosis (4).
There is a significant comorbidity of simple phobias and social phobias, as well as panic disorder.
OCD patients experience high levels of anxiety, including panic attacks, which are usually secondary to obsessive thoughts.
A characteristic feature of these panic attacks is that they are not precipitated by lactate infusion (24).
Major depressive disorder is the psychiatric condition most frequently associated with OCD, with a prevalence between 17-70%, according to different studies.
Cases of bipolar disorder have also been reported.
It is noteworthy that OCD symptoms typically improve during manic episodes and worsen during depressive episodes (4,25,26).
Obsessive-compassive personality disorder (OCPD) can be confused with OCD.
A difference lies in the fact that OCD symptoms are egodististic, while OCD symptoms are egodistic and there is no remarkable sense of intrinsic resistance.
Only 17% to 25% of OCD patients have comorbid OCD.
Other personality disorders that have been observed in OCD subjects include avoidance, histrionic and dependent personality disorders (4).
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Neuroanatomical models:
Despite the widely accepted involvement of basal ganglia in OCD (27), structural neuroimaging studies have shown few consistent changes.
Alterations in both grey matter and white matter have been described in the scientific literature; the latter have been even more widely described (28).
Recently, a diffusion tensor imaging (DTI) has detected changes in white matter in the right medial frontal and right inferior parietal regions, both in patients with OCD and in first-degree relatives (29).
On the other hand, gray matter alterations have been described in the basal ganglia, anterior cingulate cortex (ACC) and dorsolateral prefrontal cortex (DLPFC) (30).
Interest in functional neuroimaging has increased significantly.
Recent PET studies, although inconsistent (31), have detected bilateral metabolic rate, especially in the brain nuclei and caudated TOCs (32) of patients with head involvement.
Subsequent studies have shown abnormalities in the orbitofronto-striatal circuit (5.33).
Therefore, to date, the neuroanatomical model focuses on alterations in cortico-striatal connections, specifically in the orbitofronto-striatal-thalamic circuits.
It has been proposed that the orbitofrontal cortex (OFC) sends pro-neuronal projections to the head of the tail and the ventral striatum, from there to the inner pale balloon, thalamus
The hippocampus, anterior cingulate and basolateral amygdala are also part of this circuit, since they are well equipped with the COF (5).
More recently, the existence of a different neuronal circuit involving the etiology of OCD has been proposed.
Coinciding with previous findings (33), recent meta-analysis of "voxel" level analysis studies have detected alterations in the orbitofronto-striatal circuitry which also supports the detection of frontal cortex OCD in patients.
The deficits in the "set shifting", planning and inhibition of responsiveness 5.34).
This group of studies proposes the involvement of two brain circuits in the etiology of OCD.
On the one hand, the orbitofrontal-striatal circuit (and associated structures), which would be the dorsolateral prefrontal circuit), and/or the dorsolateral striatal circuit (5).
Thus, it is now proposed that the "circuity" of right-dimensional phenomena would be related to the multidimensional factors aggressive/comprobation (I) and pollution/cleaning (III), while the "spatial" circuit would be involved.
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Cognitive findings:
Very diverse cognitive deficits have been observed in OCD patients, especially in executive functions, memory, and verbal and psychomotor functions, which in turn correlate with the severity of OCD.
The COF is involved in emotional and behavioral regulation, and controls changes in the coping system.
Thus, it has been proposed that it has a specific role in the inhibition of mental illness.
The COF dysfunction causes learning deficits related to reinforcement and consequently alterations in contingencies followed by behavioral changes (5,37).
This, in turn, translates into a deficiency in behavior and an end, thus depending on the individuals of the control, habits "pre-thinking flexible guided by specific stimuli", which are triggered by specific mechanisms (41).
The involvement of the CPFDL, the CPFVL, the cingulate cortex and hippocampus contribute to executive dysfunctions: in organization, to deficits in monitoring processes and to deficits.
All this could condition the maintenance of certain behaviors (such as compulsions).
Thus, executive dysfunction becomes a key feature of OCD (37.40.42).
Some of these neuroanatomical and cognitive characteristics objectified in individuals with OCD are specifically associated with reduced activation of the lateral COF, the CPF and the left parietal cortex during cognitive inhibition and the inverse motor rigidity.
This has also been observed in unaffected relatives.
Thus, the Cambridge group proposes these findings as evidence of the existence of a specific phenotype for OCD.
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Quality of life QoL outcomes:
There is consensus on the existence of QoL affected in OCD, even informing some authors about levels lower than those observed in schizophrenia.
One study evaluated QoL in subjects with Accumulation Disorder (AD) using the short version of the Lehman Interview for Quality of Life (Lehman Quality of Life Interview-Short).
This tool measures QoL in several parameters such as: general life satisfaction; vital status; daily activities and occupational functioning; family; social relationships; economic status; work and school; legal and safety issues; and health.
It concluded that subjects with ED showed greater involvement than those with OCD in various areas, but especially in safety and housing situation.
Subjects with ED felt less confident in their neighborhoods, less protected and more vulnerable to crime (44).
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Treatment:
Many patients benefit from treatment are selective serotonin reuptake inhibitors (SSRIs), but 10-40% respond incompletely.
The early age of onset, compulsive symptoms, cleaning rituals and the long-term chronic course of the disease are poor prognostic factors that indicate a poor response to SSRIs.
The existence of a comorbid personality disorder does not influence prognosis.
Cases in which tics coexist with OCD would benefit from the addition of a neurosensory seizures (SIRSs).
Both serotonergic and dopaminergic agents are not effective in a considerable proportion of cases.
Thus, new therapeutic approaches focus on the role of glutamate and its modulation as a therapeutic option in the treatment of OCD (46).
Glutamate is the main neurotransmitter within the cortico-striate-thalamic circuit, being especially abundant in the striatum.
Thus, the scientific literature has shown that glutamatergic transmission is altered in OCD.
Established in neuroimaging studies, some researchers suggest dysregulation of this circuit.
While there is a tonic reduction of glutamate in the ACC, on the other hand there is a glutamatergic hyperactivity in the striatum and in the OFC cortex.
This finding points to the possible therapeutic action in OCD of glutamate modulating agents (47).
The specific behavioral and cognitive profile of OCD subjects can be addressed through behavioral therapy, which would also have a clear role in the management of this disorder (48).
